200 Different Cholesterol Studies
From 1988 to
Life Flow One
The Solution For Heart Disease
by
Karl Loren
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HealthGate Documents
Record 1 from database: MEDLINE
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- Title
- Pathogenesis of cholesterol gallstones.
- Author
- Hofmann AF
- Address
- Department of Medicine, University of California, San Diego, La Jolla 92093.
- Source
- J Clin Gastroenterol, 1988, 10 Suppl 2:, S1-11
- Abstract
- Symptomatic cholesterol gallstone disease occurs because of the combination
of a number of biochemical and physiologic defects: formation of supersaturated
bile, nucleation, crystal retention, stone growth, and gallbladder inflammation.
There are several possible explanations for the high prevalence of
supersaturated bile in the Western adult human as compared to other adult
mammals. First, the human liver is defective in converting cholesterol to bile
acids; the majority of cholesterol is eliminated as cholesterol. Second, the
large flux of cholesterol in vesicular form is not matched by a large flux of
recycling bile acids. Third, humans live sedentary lives and voluntarily reduce
their caloric requirement to prevent obesity. Low caloric intake decreases the
circulation of bile acids (including the flux through the hepatocyte). Fourth,
the human species is a defective bile secretor in terms of biliary volume
(microliter/kg-min) compared to other mammals. This is because human
enterohepatic circulation of bile acids is "sluggish" and because bile
acid-independent flow is also lower than in all other mammals. The accumulation
of deoxycholic acid, a secondary bile acid formed in the colon, appears to cause
secretion of bile that is supersaturated in cholesterol, and may also
contribute. Five additional risk factors explain why cholesterol gallstone
disease is so prevalent. First, the human species has a gallbladder, and the
irregular meal pattern of humans may be responsible for prolonged storage of
bile. Second, bile from cholesterol gallstone patients nucleates cholesterol
more rapidly. Third, defective gallbladder contraction is associated with
cholesterol gallstone disease in the majority of gallstone patients. Fourth, the
healthy gallbladder absorbs cholesterol and desaturates bile--protective
functions that may be lost with chronic cholecystitis. Finally, the presence of
gallstones stimulates mucous secretion, which traps cholesterol crystals.
- Language of Publication
- English
- Unique Identifier
- 89093852
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- MeSH Heading (Major)
- Bile|*; Cholelithiasis|AN/*ET; Cholesterol|*AN
- MeSH Heading
- Animal; Bile Acids and Salts|ME; Energy Intake; Human; Support, Non-U.S.
Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0192-0790
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 57-88-5 (Cholesterol)
Record 2 from database: MEDLINE
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- Title
- Structure of genes encoding steroidogenic enzymes.
- Author
- Miller WL
- Address
- Department of Pediatrics, University of California, San Francisco 94143.
- Source
- J Steroid Biochem, 1987, 27:4-6, 759-66
- Abstract
- Synthesis of adrenal steroid hormones from cholesterol entails the actions
of only five enzymes, four of which are specific forms of cytochrome P450. These
cytochrome P450 enzymes have all been isolated and their activities
reconstituted in vitro, showing that each enzyme catalyses multiple steroidal
conversions. Genes or complementary DNAs have been cloned for human P450scc (the
cholesterol side-chain cleavage enzyme), P450c17 (17 alpha-hydroxylase/17,20
lyase) and P450c21 (21-hydroxylase). The sequences for microsomal P450c17 and
P450c21 are much more closely related to one another than either is to the
sequence for mitochondrial P450scc. Each of these P450 enzymes is encoded by a
single human gene; the gene for P450scc lies on chromosome 15, that for P450c17
lies on chromosome 10, and that for P450c21 lies on chromosome 6. The human,
mouse and bovine genomes each have two P450c21 genes. While only one of these is
active in mouse and man, both genes may be active in cattle. A wide variety of
lesions in the human P450c21(B) gene causes congenital adrenal hyperplasia, a
common genetic disorder.
- Language of Publication
- English
- Unique Identifier
- 88092587
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- MeSH Heading (Major)
- Adrenal Cortex Hormones|*BI; Cytochrome P-450|*GE/ME
- MeSH Heading
- Adrenal Glands|ME; Aldehyde-Lyases|GE/ME; Animal; Base Sequence; Cattle;
Cholesterol|ME; Cholesterol Monooxygenase (Side-Chain-Cleaving)|GE/ME;
Comparative Study; DNA|GE; Human; Male; Mice; Multienzyme Complexes|GE/ME;
Progesterone Reductase|GE/ME; Sequence Homology, Nucleic Acid; Steroid
Isomerases|GE/ME; Steroid 17 alpha-Monooxygenase|GE/ME; Steroid
21-Monooxygenase|GE/ME; Testis|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0022-4731
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- EC 1.1.1.145 (Progesterone Reductase); EC 1.14.15.6 (Cholesterol
Monooxygenase (Side-Chain-Cleaving)); EC 1.14.99.10 (Steroid 21-Monooxygenase);
EC 1.14.99.9 (Steroid 17 alpha-Monooxygenase); EC 4.1.2. (Aldehyde-Lyases); EC
4.1.2.30 (17 alpha-Hydroxyprogesterone Aldolase); EC 5.3.3.- (Steroid
Isomerases); 0 (Adrenal Cortex Hormones); 0 (Multienzyme Complexes); 0 (3
beta-hydroxysteroid oxidoreductase-delta(5) 3-ketosteroid isomerase); 57-88-5
(Cholesterol); 9007-49-2 (DNA); 9035-51-2 (Cytochrome P-450)
Record 3 from database: MEDLINE
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- Title
- Probucol, high-density lipoprotein metabolism and reverse cholesterol
transport.
- Author
- Gwynne JT
- Address
- Division of Endocrinology, University of North Carolina School of Medicine,
Chapel Hill.
- Source
- Am J Cardiol, 1988 Jul 25, 62:3, 48B-51B
- Abstract
- Accumulation of cholesterol within the arterial wall reflects an imbalance
between delivery and efflux. Monocyte-derived macrophages play a major role in
arterial wall cholesterol accumulation. Using tracer methodology in a rabbit
model, several investigators have estimated the rate of cholesterol delivery and
thus the steady-state rate of efflux to be between 0.4 and 2.4
micrograms/cm2/hour. The process responsible for arterial wall cholesterol
efflux, "reverse cholesterol transport," can be conceptualized as a
sequence of events including (1) loss of cell cholesterol, (2) intravascular
cholesterol transport, (3) hepatic cholesterol uptake, and (4) biliary
secretion. Work by many investigators has characterized these individual
processes.
- Language of Publication
- English
- Unique Identifier
- 88279425
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- MeSH Heading (Major)
- Cholesterol|*ME; Lipoproteins, HDL|*ME; Phenols|*PD; Probucol|*PD
- MeSH Heading
- Animal; Arteries|DE/ME; Biological Transport|DE; Diffusion; Human;
Macrophages|DE/ME; Receptors, Cell Surface|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (HDL receptor); 0 (Lipoproteins, HDL); 0 (Phenols); 0 (Receptors, Cell
Surface); 23288-49-5 (Probucol); 57-88-5 (Cholesterol)
Record 4 from database: MEDLINE
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- Title
- Cholesterol reduction and coronary artery disease. An overview of clinical
trials up to 1986.
- Author
- Tikkanen MJ; Pyörälä K
- Address
- Third Department of Medicine, University of Helsinki, Finland.
- Source
- Drugs, 1988, 36 Suppl 3:, 27-31
- Abstract
- The 'cholesterol hypothesis' has been proven in a wealth of experimental,
clinical, genetic and epidemiological studies. Cholesterol-lowering trials
reviewed here have compared the effects of various treatment modalities on
coronary heart disease reduction. They have shown that prevention of coronary
heart disease depends on the magnitude and duration of cholesterol reduction,
not on the way it was achieved. Collective evidence from all unconfounded trials
indicates that most of the benefit of such intervention is achieved within
relatively few years of starting the intervention. With the possible exception
of adverse effects associated with clofibrate, cholesterol-lowering intervention
has not produced any untoward effects that cause concern.
- Language of Publication
- English
- Unique Identifier
- 89338072
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- MeSH Heading (Major)
- Anticholesteremic Agents|*TU; Cholesterol|*BL; Coronary Disease|*PC
- MeSH Heading
- Clinical Trials; Diet; Human; Support, Non-U.S. Gov't
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0012-6667
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Anticholesteremic Agents); 57-88-5 (Cholesterol)
Record 5 from database: MEDLINE
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- Title
- Regression of atherosclerosis.
- Author
- Arntzenius AC
- Address
-
- Source
- Horm Metab Res Suppl, 1988, 19:, 19-22
- Abstract
- The reverse of progression of atherosclerotic disease is regression of
atherosclerosis: established lesions get smaller. Animal experiments and post
mortem findings have provided investigators with considerable evidence of the
reversibility of atherosclerosis. It was, however, with arteriography in living
man, as used in prospective intervention trials, that proof was given that
atherosclerosis can be made to regress. The Leiden Intervention Trial and the
Cholesterol Lowering Atherosclerosis Study (CLAS) both have shown that with
aggressive lowering of serum cholesterol, be it with diet alone or with diet and
cholesterol-lowering drugs, atherosclerosis growth can be retarded and reversed.
The Leiden Intervention Trial and the CLAS study stress that cholesterol levels
should be lowered in angina pectoris patients and in bypassed patients, whether
their cholesterol levels are high or just slightly elevated.
- Language of Publication
- English
- Unique Identifier
- 89172810
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- MeSH Heading (Major)
- Arteriosclerosis|*TH; Atherosclerosis|BL/PA/*TH; Cholesterol|*BL
- MeSH Heading
- Animal; Body Weight; Disease Models, Animal; Human; Lipoproteins, HDL
Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0018-5043
- Country of Publication
- GERMANY, WEST
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL Cholesterol);
57-88-5 (Cholesterol)
Record 6 from database: MEDLINE
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- Title
- Coronary heart disease in hypertensives: a need to reduce cholesterol.
- Author
- Heyden S; Schneider KA; Fodor GJ
- Address
- Department of Community and Family Medicine, Duke University Medical Centre,
Durham, NC 27710.
- Source
- Int J Epidemiol, 1988 Dec, 17:4, 784-8
- Abstract
- Ten international long-term hypertension intervention trials between 1980
and 1987 have resulted in significant reduction in the incidence of stroke in
the treatment groups. Yet, eight of these studies have shown disappointing
results in the prevention of coronary heart disease (CHD). Five hypertension
intervention trials revealed high average cholesterol values at baseline. No
cholesterol treatment was provided and the incidence of CHD was high. In four
other trials with stratification into 'low' and 'high' baseline cholesterol
levels, the incidence of CHD was considerably less in the 'low' cholesterol
groups. Only the 10th, the Gothenburg trial, has demonstrated a marked reduction
in CHD by combining antihypertensive medication with cholesterol lowering
treatment. Failure to reduce cholesterol in hypertensives with
hypercholesterolaemia may be one explanation for the limited efficacy of
antihypertensive treatment in the reduction of CHD. We postulate that successful
treatment of hypercholesterolaemia will reduce the incidence of CHD in
well-controlled hypertensive patients to the same extent as it lowers the
incidence of CHD in normotensive people.
- Language of Publication
- English
- Unique Identifier
- 89138785
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|*CO/PC; Hypercholesterolemia|*CO;
Hypertension|*CO
- MeSH Heading
- Female; Human; Male
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE
- ISSN
- 0300-5771
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 7 from database: MEDLINE
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- Title
- Serum cholesterol level and the risk of colorectal cancer.
- Author
- Törnberg S
- Address
- Department of General Oncology, Karolinska Hospital, Stockholm, Sweden.
- Source
- Biomed Pharmacother, 1988, 42:6, 381-5
- Abstract
- The relation between cancer and serum cholesterol has been studied by many
scientists. In the analyses of cancers of the colon and the rectum, both
negative and positive relations to cholesterol have been described. The
divergent results may, to some extent, be explained by the use of different
statistical methods or non-comparable cohorts. A short review and discussion of
some studies dealing with the question of the relationship between serum
cholesterol and risk of cancer of the colon and the rectum is presented.
- Language of Publication
- English
- Unique Identifier
- 89118428
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Colorectal Neoplasms|*ET
- MeSH Heading
- Colonic Neoplasms|ET; Human; Rectal Neoplasms|ET; Risk Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0753-3322
- Country of Publication
- FRANCE
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 8 from database: MEDLINE
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- Title
- Mechanisms of reversed cholesterol transport.
- Author
- Small DM
- Address
- Department of Medicine, Boston University School of Medicine, Housman
Medical Research Center, Massachusetts.
- Source
- Agents Actions Suppl, 1988, 26:, 135-46
- Abstract
- Reverse cholesterol transport may be defined as the movement of cholesterol
from tissues, organs and cells to the liver (hepatocytes). Once cholesterol
enters the hepatocyte it may be catabolized to bile acids, excreted into bile as
free cholesterol, secreted back into the plasma compartment in lipoproteins or
esterified and stored in the liver. A fraction of the bile acid and cholesterol
excreted into bile is lost in the feces and accounts for the major loss of
cholesterol and its metabolites from the body. If cholesterol was not added to
the body then the mechanisms of reverse transport, bile acid and cholesterol
excretion would deplete the body of sterols. Of course the body can absorb
dietary cholesterol and synthesize cholesterol to keep overall cholesterol
homeostasis. The mechanisms of reverse transport involve 1) the physico-chemical
state of cholesterol and potential for movement within peripheral cells, tissues
and deposits (e.g., atherosclerotic plaques); 2) the net transfer of free
cholesterol from cell, tissues and deposits to acceptors (especially
lipoproteins); 3) the physical state of the acceptors (e.g., the core and
surface of lipoproteins and their capacity to accept cholesterol; 4) the LCAT
reaction; 5) the transfer proteins; 6) the lipase (LPL and HTGL) reactions; and
finally 7) the functional state of the LDL and chylomicron remnant receptors in
the liver. The net transport of cholesterol from peripheral tissues, deposits
and cells to the liver first depends on the rate of influx into the cells plus
the rate of de novo cholesterol synthesis being less than the rate of removal.
The rates of net removal will depend upon the sum of a variety of complex steps
by which cholesterol can move down a gradient to enter acceptors than be
transferred to other lipoproteins which are in turn ultimately taken up by the
liver. A potentially important fraction of cholesterol leaving cells may be
converted into cholesterol ester by LCAT then transferred to larger particles
which can then be taken up by receptor medicated endocytosis in the liver. The
HDL system must have its phospholipids replenished by both the synthesis of
nascent HDL and by the formation of phospholipid-rich surface remnants during
lipolysis of nascent triglyceride-rich lipoproteins which enter the HDL
fraction. Finally, functionally active and vigorous receptor mechanisms are
needed to remove cholesterol-containing particles into the liver.
- Language of Publication
- English
- Unique Identifier
- 89116028
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document
- MeSH Heading (Major)
- Cholesterol|*ME
- MeSH Heading
- Biological Transport; Human; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0379-0363
- Country of Publication
- SWITZERLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 9 from database: MEDLINE
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- Title
- Effects of acebutolol on the serum lipid profile.
- Author
- Clucas A; Miller N
- Address
- Rhône Poulenc Santé, Antony, France.
- Source
- Drugs, 1988, 36 Suppl 2:, 41-50
- Abstract
- Epidemiological and recent interventional studies have emphasised the
relationship between plasma lipid parameters and the incidence of coronary heart
disease. beta-Blockers, particularly those without intrinsic sympathomimetic
activity (ISA), are generally reported to increase triglyceride levels and
decrease high density lipoprotein (HDL)-cholesterol levels, both changes
theoretically increasing the risk of coronary heart disease. A review of all
published trials concerning the effects of acebutolol (a cardioselective
beta-blocker with mild ISA) on the plasma lipid profile was carried out, with a
particular emphasis on studies reporting a comparison with other beta-blockers.
The results indicate that, on average, acebutolol does not have any adverse
effects on plasma lipids and may even reduce total and low density lipoprotein
(LDL)-cholesterol by 7 and 5%, respectively. In contrast, the other
beta-blockers compared under the same conditions (propranolol, pindolol and
penbutolol) tended to increase triglyceride levels (+19% when compared with
acebutolol) and decrease HDL-cholesterol (-7% when compared with acebutolol) to
an extent that was consistent with previous reports in the literature. In
interpreting these differences in lipid parameters in the light of
epidemiological and interventional study data, the use of acebutolol as opposed
to the other beta-blockers could theoretically lead to a relative reduction in
coronary risk of 20% or more.
- Language of Publication
- English
- Unique Identifier
- 89106964
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- MeSH Heading (Major)
- Acebutolol|AE/*PD; Cholesterol|*BL; Lipoproteins|*BL; Triglycerides|*BL
- MeSH Heading
- Comparative Study; Human; Penbutolol|PD; Pindolol|PD; Propranolol|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0012-6667
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 0 (Triglycerides); 13523-86-9 (Pindolol); 36507-48-9
(Penbutolol); 37517-30-9 (Acebutolol); 525-66-6 (Propranolol); 57-88-5
(Cholesterol)
Record 10 from database: MEDLINE
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- Title
- Effects of diuretic drugs on the lipid profile.
- Author
- Ames R
- Address
- St Luke's-Roosevelt Hospital, New York, New York.
- Source
- Drugs, 1988, 36 Suppl 2:, 33-40
- Abstract
- Thiazide-type diuretic drugs modify the lipoprotein profile when used in the
short term treatment of hypertension. Total cholesterol increases by 6 to 7% on
average because of raised concentrations of low density or very low density
lipoprotein cholesterol or both. High density lipoprotein cholesterol does not
change. Spironolactone has a lesser effect on lipids than do thiazides. In
contrast, the methylindoline compound, indapamide, a diuretic with vasodilator
activity, has produced no adverse effects on lipids or lipoproteins. Long term
data on thiazide monotherapy are sparse but suggest a persistence of the lipid
effect for as long as 6 years of treatment. The clinical impact of these lipid
changes is unclear. Although clinical trials have proved the benefit of lowering
cholesterol on the incidence of coronary heart disease, the clinical
significance of these diuretic-induced increases is unknown. A clinical trial
will be required to resolve the issue by comparing antihypertensive drugs with
and without adverse effects on the lipid profile. Because coronary heart disease
is the most common complication of mild hypertension, and as diuretic-based
regimens have not succeeded in curbing it, resolution of this concern is
important.
- Language of Publication
- English
- Unique Identifier
- 89106963
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Diuretics, Thiazide|*PD; Lipoproteins|*BL;
Triglycerides|*BL
- MeSH Heading
- Drug Combinations; Human; Hypertension|BL/DT; Indapamide|PD; Potassium|BL;
Spironolactone|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0012-6667
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Diuretics, Thiazide); 0 (Drug Combinations); 0 (Lipoproteins); 0
(Triglycerides); 26807-65-8 (Indapamide); 52-01-7 (Spironolactone); 57-88-5
(Cholesterol); 7440-09-7 (Potassium)
Record 11 from database: MEDLINE
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- Title
- Adaptive changes in aging and arteriosclerosis--role of cholesterol.
- Author
- Kaunitz H
- Address
- Department of Pathology, Columbia University, New York, NY 10032.
- Source
- Mech Ageing Dev, 1988 Jul, 44:1, 35-43
- Abstract
- The "lipid theory" assumes that cholesterol has a causal part in
the development of arteriosclerosis; however, in view of the fact that
cholesterol has always accompanied life processes, the "lipid theory"
contradicts the evolutionary principle of "teleonomy" which predicts
that long lasting metabolic effects must have beneficial consequences. Support
for the theory was claimed from the correlation between high serum cholesterol
and arteriosclerotic complications, from observations in cholesterol fed animals
and from cardiac lesions in familial hypercholesterolemia. However, correlations
do not prove causality; whether the animal experiments and the observations in
familial hypercholesterolemia are pertinent is questionable. Therefore, the
possibility was considered that the cholesterol changes are an adaptive
mechanism. This is supported by the "normal" cholesterol content of
the early lesion, by the stabilization of the DNA helix by cholesterol in
appropriate concentration, by the beneficial effects of cholesterol-rich
granulomata; by recent reliable "intervention" trials with low
cholesterol diets and by the observation that persons dying from ischemic heart
disease (having high serum cholesterol) live at least as long as those dying
from other causes. Furthermore, studies with serum cholesterol lowering drugs
are difficult to interpret and often misleading. The symptomatology of the serum
cholesterol changes in arteriosclerosis suggests that they belong to the
adaptive aging phenomenon. This would be in line with evolutionary thinking.
- Language of Publication
- English
- Unique Identifier
- 89082082
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- MeSH Heading (Major)
- Aging|*; Arteriosclerosis|ET/*PP; Cholesterol|*PH
- MeSH Heading
- Human; Lipids|PH
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0047-6374
- Country of Publication
- SWITZERLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 12 from database: MEDLINE
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- Title
- Discovery, biochemistry and biology of lovastatin.
- Author
- Alberts AW
- Address
- Merck Sharp & Dohme Research Laboratories, Department of Biochemical
Regulation, Rahway, New Jersey 07065.
- Source
- Am J Cardiol, 1988 Nov 11, 62:15, 10J-15J
- Abstract
- Cholesterol is a 27-carbon steroid that is an essential component of the
cell membrane, the immediate precursor of steroid hormones, the substrate for
the formation of bile acids, and is required for the assembly of very low
density lipoprotein in the liver. Because as much as two-thirds of total body
cholesterol in patients is of endogenous origin, an effective means to control
cholesterogenesis may occur by inhibition of its biosynthesis. Cholesterol is
biosynthesized in a series of more than 25 separate enzymatic reactions that
initially involve the formation of 3-hydroxy-3-methylglutaryl coenzyme A (HMG
CoA). Early attempts to pharmacologically block cholesterol synthesis focused
only on steps later in the biosynthetic pathway and resulted in compounds with
unacceptable toxicity. Recent research had identified that HMG CoA reductase is
a key rate-limiting enzyme in this pathway and is responsible for the conversion
of HMG CoA to mevalonate. Additional research with fungal metabolites identified
a series of compounds with potent inhibiting properties for this target enzyme,
from which lovastatin was selected for clinical development. A reduction in
cholesterol synthesis by lovastatin has been subsequently confirmed in cell
culture, animal studies and in humans. A resultant decrease in circulating total
and low-density lipoprotein (LDL) cholesterol has also been demonstrated in
animals and humans. Because hepatic LDL receptors are the major mechanism of LDL
clearance from the circulation, further animal research has confirmed that these
declines in cholesterol are accompanied by an increase in hepatic LDL receptor
activity. Lovastatin effectively diminishes endogenous cholesterol synthesis
providing useful therapeutic properties for patients with hypercholesterolemia.
- Language of Publication
- English
- Unique Identifier
- 89047165
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- MeSH Heading (Major)
- Hydroxymethylglutaryl CoA Reductases|*AI; Hypercholesterolemia|*DT;
Lovastatin|*/PD/TU
- MeSH Heading
- Animal; Chemistry; Cholesterol|BI; Human; Liver|ME; Receptors, LDL|DE
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 1.1.1.88 (Hydroxymethylglutaryl CoA Reductases); 0 (Receptors, LDL);
57-88-5 (Cholesterol); 75330-75-5 (Lovastatin)
Record 13 from database: MEDLINE
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- Title
- Cholesterol emboli after cardiac catheterization. Eight cases and a review
of the literature.
- Author
- Colt HG; Begg RJ; Saporito JJ; Cooper WM; Shapiro AP
- Address
- Department of Medicine, Shadyside Hospital, Pittsburgh, Pennsylvania 15232.
- Source
- Medicine (Baltimore), 1988 Nov, 67:6, 389-400
- Abstract
- Cholesterol embolization is a puzzling event that may be increasingly
iatrogenic in origin. Diagnosis is difficult and requires a high index of
suspicion, an appropriate clinical picture, and usually, confirmation by biopsy.
Certain laboratory abnormalities may be helpful; the elevated sedimentation rate
and relative eosinophilia found in our patients concurs with other cases
reported in the literature. Prognosis is related to the extent of systemic
involvement, but renal disease is particularly threatening and gangrene and
infection can be lethal. Multiple therapeutic regimens have been generally
unsuccessful in altering the course of the disease process. The most significant
impact on the disease can be made by its prevention. Cholesterol emboli occur
spontaneously, but also after invasive aortic procedures such as diagnostic
angiography or cardiovascular surgery. In addition, cardiac catheterization and
percutaneous transluminal coronary angioplasty have the potential for arterial
trauma and consequent cholesterol embolization. Although the apparent increasing
numbers of cholesterol emboli may be a reflection of the increased use of
arterial invasive procedures, they are being performed on an older, more
severely ill population, with other risk factors for the development of embolic
phenomena, i.e., age, smoking history, diabetes mellitus, hypertension, and
peripheral vascular disease. Our observed cases and review of the literature do
not furnish information concerning the comparative incidences of embolization as
related to the suggested etiologies. Careful documentation of the clinical
situation preceding the event, the type of procedure, the site of arterial
entry, and the duration, difficulty, and extent of the intravascular invasion
(i.e., above or below the left subclavian artery) are necessary for this
purpose. Such data should help to develop guidelines for patient and procedure
selection in order to minimize the possibility of cholesterol embolization.
- Language of Publication
- English
- Unique Identifier
- 89039240
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- MeSH Heading (Major)
- Cholesterol|*; Embolism|*ET; Heart Catheterization|*AE
- MeSH Heading
- Aged; Case Report; Female; Human; Male; Middle Age
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE
- ISSN
- 0025-7974
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 14 from database: MEDLINE
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- Title
- Multiple cholesterol emboli syndrome complicating angiographic techniques.
- Author
- Palmer FJ; Warren BA
- Address
- Department of Radiology, Prince Henry Hospital, Sydney, Australia.
- Source
- Clin Radiol, 1988 Sep, 39:5, 519-22
- Abstract
- Three cases of widespread microembolisation of cholesterol crystals
following angiography are described. The multiple cholesterol emboli syndrome
has been well described as a spontaneous phenomenon and it is surprising that
its occurrence during angiography appears rare. Only 19 cases could be found in
the literature and these are reviewed. Dissemination of particulate cholesterol
material produces irreversible organ ischaemia when a threshold 'dose' is
reached. Males and patients with clinical evidence of widespread atherosclerosis
are at increased risk. Prognosis is poor and available therapy unsatisfactory.
- Language of Publication
- English
- Unique Identifier
- 89029526
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document
- MeSH Heading (Major)
- Angiography|*AE; Cholesterol|*; Embolism|*ET
- MeSH Heading
- Aged; Case Report; Human; Male; Middle Age; Syndrome
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES
- ISSN
- 0009-9260
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 15 from database: MEDLINE
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- Title
- European Consensus on Primary Prevention of Coronary Heart Disease.
- Author
- Assmann G
- Address
- Central Laboratory Institute for Clinical Chemistry, Westfalische Wilhelms
Universitat Münster, West Germany.
- Source
- Can J Cardiol, 1988 Jul, 4 Suppl A:, 21A-23A
- Abstract
- The European Consensus on Primary Prevention of Coronary Heart Disease has
recommended that providing care for individuals at particular risk for coronary
artery disease (CAD) requires case finding through medical examinations in
primary care, hospital and employment health examination settings. Decisions
concerning management of elevated lipid levels should be based on overall
cardiovascular risk. The goal of reducing cholesterol levels through risk
reduction can ultimately be accomplished only with the implementation of health
education efforts directed toward all age groups and actions by government and
supranational agencies, including adequate food labelling to identify fat
content, selective taxation to encourage healthful habits and wider availability
of exercise facilities. Only measures directed at the overall population can
eventually reach the large proportion of individuals at mildly to moderately
increased risk for CAD. The European Policy Statement on the Prevention of
Coronary Heart Disease recognizes that the question of lipid elevation as a risk
factor for CAD involves assessment, not only of cholesterol level alone, but
also of triglycerides and the HDL cholesterol lipid fraction. Five specific
categories of dyslipidemia have been identified, with individualized screening
and treatment strategies advised for each. It is the consensus of the study
group panel members that these procedures are both practical and feasible. They
begin the necessary long term process to reduce the unacceptably high levels of
morbidity and mortality due to CAD throughout the European community.
- Language of Publication
- English
- Unique Identifier
- 89027866
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document
- MeSH Heading (Major)
- Coronary Disease|*PC
- MeSH Heading
- Cholesterol|BL; Europe; Human; Hyperlipidemia|PC; Lipoproteins, HDL
Cholesterol|BL; Risk Factors
- Publication Type
- CONSENSUS DEVELOPMENT CONFERENCE; JOURNAL ARTICLE; REVIEW; REVIEW LITERATURE
- ISSN
- 0828-282X
- Country of Publication
- CANADA
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 57-88-5 (Cholesterol)
Record 16 from database: MEDLINE
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- Title
- Coronary prevention and regression studies updated.
- Author
- Little JA
- Address
- Department of Medicine, St Michael's Hospital, Toronto, Ontario.
- Source
- Can J Cardiol, 1988 Jul, 4 Suppl A:, 11A-15A
- Abstract
- There have been a multitude of clinical, animal and epidemiology studies
which prove that high serum cholesterol and low density lipoprotein (LDL)
cholesterol concentrations are specific causes of coronary artery disease (CAD).
Although the variations in experimental design make comparisons difficult, the
aggregate results of many human prevention trials since 1960 lead to the
definite conclusion that a 10% lowering of serum cholesterol reduces the risk of
CAD by one-sixth. Recently, other factors for CAD risk have been identified that
will be useful in guiding treatment, namely serum high density lipoprotein (HDL)
cholesterol, apolipoproteins B and AI, HDL triglycerides and phosphatidylcholine
to free cholesterol ratio. Studies have shown that aggressive drug and diet
therapy slows progression and causes regression of atheromas. Primary prevention
of CAD is obviously preferable to secondary prevention. Also, the evidence to
date indicates that prevention of CAD through lifestyle changes should begin in
childhood.
- Language of Publication
- English
- Unique Identifier
- 89027864
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|*PC
- MeSH Heading
- Clinical Trials; Coronary Arteriosclerosis|PC; Human; North America; Risk
Factors
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE
- ISSN
- 0828-282X
- Country of Publication
- CANADA
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 17 from database: MEDLINE
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- Title
- Atherosclerosis and apoprotein E. An enigmatic relationship.
- Author
- Getz GS; Mazzone T; Soltys P; Bates SR
- Address
- Department of Pathology, University of Chicago, IL 60637.
- Source
- Arch Pathol Lab Med, 1988 Oct, 112:10, 1048-55
- Abstract
- In this article, we consider the role of apoprotein E in lipoprotein
metabolism and especially in the metabolism of potentially atherogenic
lipoproteins. Particular consideration has been given to three features of
apoprotein E involvement in lipid cell interactions. Evidence implicating free
cholesterol as a mediator of apoprotein E biosynthesis in cholesterol-loaded
macrophages is presented. Experiments pointing to apoprotein E as the ligand
promoting the interaction of beta-very-low-density lipoprotein (beta-VLDL) with
macrophages are summarized. Finally, we describe the influence of fat and
cholesterol fed to rhesus monkeys and baboons on the generation of hepatogenous
(from isolated liver perfusates) VLDL enriched in cholesterol ester and
apoprotein E. These hepatic VLDLs, none of which exhibits beta-electrophoretic
mobility, promote cholesterol esterification in macrophages in proportion to
their apoprotein E content. The complex role of apoprotein E in the genesis and
reversal of atherosclerosis is briefly discussed.
- Language of Publication
- English
- Unique Identifier
- 89025045
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document
- MeSH Heading (Major)
- Apolipoproteins E|BI/ME/*PH; Arteriosclerosis|*ET; Atherosclerosis|*ET
- MeSH Heading
- Animal; Cholesterol|BL/ME; Esterification; Human; Lipoproteins, VLDL|ME;
Macrophages|ME; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0003-9985
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins E); 0 (Lipoproteins, VLDL); 57-88-5 (Cholesterol)
Record 18 from database: MEDLINE
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- Title
- Assessing and managing hyperlipidemia.
- Author
- Crouch MA
- Address
- Department of Family Medicine and Comprehensive Care, Louisiana State
University Medical Center, School of Medicine, Shreveport.
- Source
- J Am Board Fam Pract, 1988 Jul-Sep, 1:3, 175-88
- Abstract
- Because more than one-half of adult Americans have total blood cholesterol
levels that often contribute to atherosclerotic blockage of their coronary
arteries, routine random screening of all adults and high-risk children for
hypercholesterolemia is recommended. Reduced intake of saturated fat and
cholesterol can lower total and low-density lipoprotein (LDL) cholesterol by
10-20 percent, while several medications lower total and LDL cholesterol by
15-40 percent. A highly effective cholesterol-lowering medication, lovastatin,
has been recently marketed. The efficacy and long-term safety of ingesting large
amounts of omega-3 fatty acids in fish oil supplements are unproven.
Hypercholesterolemia is a family problem transmitted between generations by
various combinations of genetic factors and learned behaviors. The family
physician can be most effective by working with entire families to detect and
treat hypercholesterolemia early in life to prevent serious consequences of
prolonged cholesterol elevation.
- Language of Publication
- English
- Unique Identifier
- 89022187
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document
- MeSH Heading (Major)
- Hyperlipidemia|BL/DH/DT/*PC
- MeSH Heading
- Antilipemic Agents|TU; Cholesterol|BL; Dietary Fats, Unsaturated|TU; Human;
Life Style; Mass Screening; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0893-8652
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antilipemic Agents); 0 (Dietary Fats, Unsaturated); 0 (Triglycerides);
57-88-5 (Cholesterol)
Record 19 from database: MEDLINE
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- Title
- Bilateral cholesterol granuloma of the skull base: case report and review of
the literature.
- Author
- Gamache FW Jr; McLure T; Deck M; Linstrom C
- Address
- Department of Neurosurgery, Cornell University Medical College, The New York
Hospital, New York.
- Source
- Neurosurgery, 1988 Jun, 22:6 Pt 1, 1098-101
- Abstract
- A unique case of bilateral cholesterol granuloma of the skull base and its
treatment is presented. Cholesteatoma, a pathological entity often confused with
cholesterol granuloma, is differentiated from cholesterol granuloma. Cholesterol
granuloma is not rare. This tumor seems to derive from an inflammatory process
at the skull base that results in bony erosion surrounding a cyst wall of
inflammatory tissue. Neurological abnormalities reflect the location of the
tumor in relation to the brain stem. Radiographically, the cyst wall enhances
with the administration of i.v. contrast agent, and the center of the lesion is
isodense with brain on computed tomography, unlike cholesteatoma. Magnetic
resonance imaging characteristics are currently being defined. At operation,
cholesterol granuloma consists primarily of a viscous fluid within a capsule of
inflammatory tissue. Treatment requires establishing a pathway for drainage of
the granuloma. The advantages of transsphenoidal, transclival drainage of such
lesions are outlined.
- Language of Publication
- English
- Unique Identifier
- 88334862
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document
- MeSH Heading (Major)
- Bone Diseases|*DI/ME/SU; Cholesterol|*AN; Granuloma|*DI/ME/SU; Magnetic
Resonance Imaging|*; Skull|*RA/SU
- MeSH Heading
- Adult; Case Report; Female; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES
- ISSN
- 0148-396X
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 20 from database: MEDLINE
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- Title
- Physiological and pharmacological regulation of small intestinal cholesterol
synthesis.
- Author
- Strandberg TE; Tilvis RS
- Address
- Second Department of Medicine, University of Helsinki, Finland.
- Source
- Gen Pharmacol, 1988, 19:3, 321-9
- Abstract
- 1. The small intestine is an important site of cholesterol synthesis in the
body and at least in experimental animals, it also contributes to the
circulating plasma pool of cholesterol. 2. Studies on synthesis regulation have
been partly contradictory but it is now concluded that the cellular cholesterol
balance is the basic regulatory factor of intestinal cholesterol synthesis.
However, the balance is affected differently in various specialized cells and
parts of the small intestine. 3. Most data on synthesis regulation are derived
from experimental animals but the few human studies suggest that similar
regulatory factors function in man, too.
- Language of Publication
- English
- Unique Identifier
- 88329608
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document
- MeSH Heading (Major)
- Cholesterol|*BI/BL; Intestinal Mucosa|DE/*ME; Intestine, Small|DE/*ME
- MeSH Heading
- Animal; Antilipemic Agents|PD; Bile Acids and Salts|ME; Cell Cycle;
Circadian Rhythm; Diet; Fasting; Hormones|PH; Human; Lipoproteins|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0306-3623
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Antilipemic Agents); 0 (Bile Acids and Salts); 0 (Hormones); 0
(Lipoproteins); 57-88-5 (Cholesterol)
Record 21 from database: MEDLINE
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- Title
- Labeling of participants in high blood pressure screening programs.
Implications for blood cholesterol screenings.
- Author
- Lefebvre RC; Hursey KG; Carleton RA
- Address
- Division of Health Education, Memorial Hospital of Rhode Island, Pawtucket
02860.
- Source
- Arch Intern Med, 1988 Sep, 148:9, 1993-7
- Abstract
- Screening programs have expanded to identify the many persons who are
unaware of their high blood cholesterol level and thus are at an increased risk
for coronary heart disease. These programs bring both potential benefits and
potential risks to the participant. One potential risk is that of iatrogenic
effects of learning one's risk status, often referred to as the "labeling
phenomenon." Research that has addressed the labeling phenomenon in blood
pressure screening programs has important implications for blood cholesterol
screenings. Detrimental effects on screening participants are possible, but they
can be attenuated by careful attention to characteristics of the debriefing and
counseling that should be included in screening protocols.
- Language of Publication
- English
- Unique Identifier
- 88325754
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document
- MeSH Heading (Major)
- Blood Pressure Determination|*; Cholesterol|*BL; Hypertension|CO/EP/*PX;
Mass Screening|*; Sick Role|*
- MeSH Heading
- Absenteeism; Counseling; Evaluation Studies; Human;
Hypercholesterolemia|BL/CO/EP/PX; Life Style; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0003-9926
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 22 from database: MEDLINE
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- Title
- Cholesterol gallstone disease: the current status of nonsurgical therapy.
- Author
- Bilhartz LE
- Address
- Department of Medicine, University of Texas Southwestern Medical Center,
Dallas 75235-9030.
- Source
- Am J Med Sci, 1988 Jul, 296:1, 45-56
- Abstract
- Gallstone disease is a common disease that appears to be related to a
Western diet. The underlying pathogenesis is a subtle alteration in the liver
such that excessive cholesterol is extracted from the liver cell by bile acids
undergoing an enterohepatic recirculation. Gallstone disease progresses through
well-defined stages, beginning with a bile supersaturated with cholesterol and
proceeding to crystal formation, stone growth, and finally symptoms caused by
impaction of a stone in either the cystic duct or the common bile duct. The
natural history is that most stones never cause symptoms. Stones that cause
symptoms have been present for an average of 12 years. The treatment of truly
asymptomatic stones should be observation. Ultrasonography of the right upper
quadrant is the gold standard for the diagnosis of stones in the gallbladder.
Endoscopic retrograde cholangiopancreatography (ERCP) is the gold standard for
the diagnosis of stones in the common bile duct. Oral cholecystogram (OCG) helps
select patients who have noncalcified, floating stones that may be dissolved
with bile acids or methyl tertiary butyl ether (MTBE). Therapy with chenodiol
has been a disappointment because of a low complete response rate. The ideal
candidate for attempted dissolution with chenodiol would be a thin woman with
hypercholesterolemia and a small number of symptomatic, small, floating,
radiolucent gallstones. Ursodeoxycholic acid (Urso), when it is available, will
have all of the attributes of chenodiol and virtually none of the side effects.
Rapid dissolution of gallstones with MTBE shows great promise of being a
generally available means of dissolving gallstones. Extracorporeal shock wave
lithotripsy also shows promise, but its general availability may be limited by
the cost of the equipment needed. As of now, the treatment of choice for
symptomatic gallstones remains cholecystectomy, unless there is a compelling
reason not to operate.
- Language of Publication
- English
- Unique Identifier
- 88307464
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document
- MeSH Heading (Major)
- Cholelithiasis|AN/*TH; Cholesterol|*AN
- MeSH Heading
- Chenodeoxycholic Acid|TU; Cholecystectomy; Ethers|TU; Human; Lithotripsy;
Risk Factors; Solvents|TU; Support, Non-U.S. Gov't; Ursodeoxycholic Acid|TU
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9629
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Ethers); 0 (Solvents); 128-13-2 (Ursodeoxycholic Acid); 1634-04-4 (methyl
tert-butyl ether); 474-25-9 (Chenodeoxycholic Acid); 57-88-5 (Cholesterol)
Record 23 from database: MEDLINE
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- Title
- Reliability of lipid, lipoprotein, and apolipoprotein measurements.
- Author
- Naito HK
- Address
- Department of Biochemistry, Cleveland Clinic Foundation, OH 44195.
- Source
- Clin Chem, 1988, 34:8B, B84-94
- Abstract
- The National Heart, Lung, and Blood Institute national awareness program on
cholesterol and heart disease has placed new demands on laboratorians to utilize
and perform more reliable measurements of lipids, lipoproteins, and
apolipoproteins. The general public's awareness and the clinicians' concerns
about the reliability of laboratory testing make it paramount that the
analytical problems and issues are identified and solutions are provided to
increase the current state of reliability of the measurement of these blood
constituents. To accomplish this, the initial step is to assess the current
state of reliability of lipid, lipoprotein, and apolipoprotein measurements in
the clinical laboratories. Accuracy and precision of measurements of total
cholesterol, triglycerides, high-density lipoprotein cholesterol, and
apolipoproteins A-I and B are extensively discussed, and general as well as some
specific recommendations are provided for some of the apparent problems.
- Language of Publication
- English
- Unique Identifier
- 88295453
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document
- MeSH Heading (Major)
- Apolipoproteins|*BL; Lipids|*BL; Lipoproteins|*BL
- MeSH Heading
- Autoanalysis; Cholesterol|BL; Human; Lipoproteins, HDL|BL; Lipoproteins, HDL
Cholesterol|BL; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0009-9147
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins); 0 (Lipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0
(Lipoproteins, HDL); 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 24 from database: MEDLINE
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- Title
- Cholesterol, lipoproteins, and coronary heart disease in women.
- Author
- Bush TL; Fried LP; Barrett-Connor E
- Address
- Department of Epidemiology, Johns Hopkins University, School of Hygiene and
Public Health, Baltimore, MD.
- Source
- Clin Chem, 1988, 34:8B, B60-70
- Abstract
- In the United States, coronary heart disease is the major cause of death and
disability in women and in men. Despite this, little is known about the risk
factors, including cholesterol and lipoprotein concentrations, for coronary
disease in women. In this paper we review the determinants of cholesterol and
lipoprotein concentrations in women, assess whether values for total cholesterol
and lipoproteins (HDL and LDL) are associated with the occurrence of coronary
heart disease in women, and evaluate the evidence that suggests that modifying
the concentrations of lipids in women is associated with changing the risk of
coronary disease. Besides genetic determinants, dietary cholesterol, dietary
fat, total caloric intake, alcohol consumption, cigarette smoking, and physical
activity are known to influence concentrations of lipids in women. Some of the
strongest determinants of cholesterol and lipoprotein concentrations in women
are sex hormones, including estrogen and progestin. Exogenous use of both of
these hormones markedly influences HDL and LDL cholesterol; additional evidence
suggests that endogenous sex hormones also influence lipid and lipoprotein
concentrations. The few studies that have examined the association of total
cholesterol with coronary heart disease occurrence and mortality in women have
consistently shown that (a) women have much lower rates of coronary heart
disease than men at the same values for cholesterol, and (b) clearly elevated
risk for coronary heart disease in women is evident only at relatively high
values of total cholesterol (i.e., greater than 260 mg/dL). There also appears
to be an age effect, with total cholesterol concentrations being more predictive
in older than in younger women.
- Language of Publication
- English
- Unique Identifier
- 88295450
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|BL/*EP/GE/MO; Lipoproteins|*BL
- MeSH Heading
- Adult; Age Factors; Aged; Contraceptives, Oral, Hormonal|AE; Epidemiologic
Methods; Female; Human; Male; Menopause; Middle Age; Risk Factors; Sex Factors;
United States
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0009-9147
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 57-88-5 (Cholesterol)
Record 25 from database: MEDLINE
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- Title
- Cholesterol and risk of coronary heart disease and mortality in men.
- Author
- Kannel WB
- Address
- Section of Preventive Medicine and Epidemiology, Boston University School of
Medicine, MA.
- Source
- Clin Chem, 1988, 34:8B, B53-9
- Abstract
- Extensive data implicate cholesterol in the atherosclerotic process
responsible for coronary disease. Of the atherosclerotic disease outcomes, serum
cholesterol is most strongly related to coronary disease. A significant
relationship of serum cholesterol to all clinical manifestations of coronary
heart disease has been demonstrated in the Framingham Study, after adjusting for
coexistent risk factors. Cholesterol and blood pressure exert similar influences
on the occurrence of coronary heart disease. Risk of coronary heart disease
associated with serum cholesterol is continuous, graded, and strong, with ideal
values for cholesterol probably in the 130-190 mg/dL range. The impact of serum
cholesterol diminishes with advancing age, but the predictive value of
cholesterol is restored when fractionated into its atherogenic LDL and
protective HDL components. The predictive value of total cholesterol in serum at
all concentrations, including values less than 200 mg/dL, can be enhanced by
taking HDL cholesterol into account. The total/HDL cholesterol ratio is a
practical, efficient means for evaluating the joint effect of the two-way
cholesterol traffic. Other cardiovascular risk factors such as blood pressure,
glucose, cigarette smoking, fibrinogen, and left ventricular hypertrophy
markedly influence the risk associated with measured concentrations of serum
cholesterol. In correcting hypertension or diabetes, lipid values are an
important consideration in determining the urgency, type, and efficacy of
treatment used. In contrast to coronary mortality, rates of overall mortality
show a quadratic relationship to total cholesterol in serum, with excessive
mortality at concentrations greater than 160 mg/dL.
- Language of Publication
- English
- Unique Identifier
- 88295449
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|BL/EP/*MO
- MeSH Heading
- Adult; Age Factors; Aged; Epidemiologic Methods; Female; Human;
Lipoproteins|BL; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL
Cholesterol; Male; Middle Age; Risk Factors; United States
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0009-9147
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL
Cholesterol); 57-88-5 (Cholesterol)
Record 26 from database: MEDLINE
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- Title
- Chemistry, biochemistry, and pharmacology of HMG-CoA reductase inhibitors.
- Author
- Endo A
- Address
- Department of Agricultural and Biological Chemistry, Tokyo Noko University,
Japan.
- Source
- Klin Wochenschr, 1988 May 16, 66:10, 421-7
- Abstract
- After an extensive searching for a microbial product that inhibits
cholesterol synthesis, compactin and a series of related metabolites like
monacolin K (mevinolin) have been isolated from molds as active agents. These
compounds, which were structurally related to hydroxymethylglutaryl coenzyme A,
were potent competitive inhibitors of hydroxymethylglutaryl coenzyme A
reductase, the rate-limiting enzyme in cholesterol synthesis. The inhibition was
reversible and the inhibitor constant Ki for compactin was around 10(-9) M.
Compactin inhibited cholesterol synthesis in mammalian cells at 10(-9) M. Sterol
synthesis in vivo was also reduced when compactin was given orally to rats at a
dose of 50 mg/kg. Hydroxymethylglutaryl coenzyme A reductase activity of both
cultured cells and rat liver was elevated when sterol synthesis was strongly
inhibited by compactin. Both the growth inhibition and reductase induction could
be overcome by the presence of mevalonate. A compactin-resistant cell line of
mouse FM3A cells, called CR200, was developed by stepwise selection. CR200-cells
had an abnormally high level of reductase activity and amplified reductase gene.
Compactin was not able to lower plasma cholesterol levels in mice, rats, and
hamsters. However, it was highly effective in rabbits, dogs, and monkeys; plasma
cholesterol of dogs was reduced by 30%-40% at a dose of 20-50 mg/kg. The
low-density lipoprotein cholesterol, which is responsible for atherosclerosis,
was preferentially lowered. Compactin was also highly effective in
hypercholesterolemic patients at a small dose. The results of the current
studies have proved that compactin and related compounds are far more effective
in lowering plasma cholesterol than any other drugs available.(ABSTRACT
TRUNCATED AT 250 WORDS)
- Language of Publication
- English
- Unique Identifier
- 88287301
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Hydroxymethylglutaryl CoA Reductases|*AI; Liver|*DE/EN
- MeSH Heading
- Animal; Chemistry; Human; Hypercholesterolemia|DT; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0023-2173
- Country of Publication
- GERMANY, WEST
- CAS Registry/EC Number
- EC 1.1.1.88 (Hydroxymethylglutaryl CoA Reductases); 57-88-5 (Cholesterol)
Record 27 from database: MEDLINE
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- Title
- Biliary cholesterol and lithogeneity of bile in patients after ileal
resection.
- Author
- Färkkilä MA
- Address
- Second Department of Medicine, University of Helsinki, Finland.
- Source
- Surgery, 1988 Jul, 104:1, 18-25
- Abstract
- For determination of the factors that regulate biliary cholesterol secretion
and the lithogenity of bile in ileal dysfunction, plasma and biliary lipids and
fecal excretion of bile acids were studied in 29 patients who had undergone
ileal resection. Seven patients with ileal resection had normal bile acid
excretion (less than 10 mg/kg/day), and 22 had various degrees of bile acid
malabsorption. None of the patients had gallstones when examined with abdominal
sonography. LDL cholesterol levels were decreased in bile acid malabsorption and
demonstrated a positive correlation with the molar percentage of biliary
cholesterol. Biliary cholesterol (mol percent) was inversely correlated with
fecal bile acid excretion. This finding suggests that biliary cholesterol
secretion decreases with increasing loss of bile acids to feces in ileal
dysfunction, leading to an actual decrease in the lithogenic index and to
hyposaturation of cholesterol in bile. The reduction in biliary cholesterol,
regarded as protecting the gallbladder mucosa against the detergent properties
of bile acids, may play an important role in the pathogenesis of increased
gallstone formation in ileal dysfunction.
- Language of Publication
- English
- Unique Identifier
- 88264723
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document
- MeSH Heading (Major)
- Bile|*AN; Cholelithiasis|*ME; Cholesterol|*SE; Ileum|*SU
- MeSH Heading
- Bile Acids and Salts|ME; Feces|AN; Human; Lipids|AN; Malabsorption
Syndromes|ME; Male; Middle Age; Postoperative Period; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0039-6060
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 57-88-5 (Cholesterol)
Record 28 from database: MEDLINE
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- Title
- Serum cholesterol and risk of cancer in a cohort of 39,000 men and women.
- Author
- Knekt P; Reunanen A; Aromaa A; Heliövaara M; Hakulinen T; Hakama M
- Address
- Social Insurance Institution, Helsinki, Finland.
- Source
- J Clin Epidemiol, 1988, 41:6, 519-30
- Abstract
- Serum cholesterol concentration was studied for its prediction of cancer in
39,268 men and women aged 15-99 years and initially free from cancer. During a
median follow-up of 10 years 1381 cancer cases were diagnosed. Serum cholesterol
level was inversely associated with cancer incidence among non-smokers.
Age-adjusted relative risks of cancer in quintiles of serum cholesterol were in
male non-smokers 1.0, 0.81, 0.73, 0.69, and 0.46 and in female non-smokers 1.0,
0.75, 0.84, 0.78, and 0.70. The associations were not found to be confounded by
serum vitamins A or E, serum selenium or several other factors. The association
between serum cholesterol level and risk of cancer varied from strongly negative
to slightly positive according to subpopulation and site of cancer. The
strongest negative associations were found to appear during the first years of
follow-up, especially for rapidly developing cancers. Thus the increased
occurrence of cancer at low cholesterol levels seems mainly to be due to
preclinical cancer.
- Language of Publication
- English
- Unique Identifier
- 88258552
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Neoplasms|*BL/EP/ET
- MeSH Heading
- Adolescence; Adult; Aged; Aged, 80 and over; Colonic Neoplasms|BL; Female;
Finland; Follow-Up Studies; Human; Male; Middle Age; Precancerous Conditions|BL;
Prostatic Neoplasms|BL; Questionnaires; Random Allocation; Registries; Risk
Factors; Sampling Studies; Sex Factors; Smoking|BL; Vitamin A|BL; Vitamin E|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0895-4356
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 11103-57-4 (Vitamin A); 1406-18-4 (Vitamin E); 57-88-5 (Cholesterol)
Record 29 from database: MEDLINE
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- Title
- Risk factor modification trials: implications for the elderly.
- Author
- Stamler J
- Address
- Department of Community Health and Preventive Medicine, Northwestern
University Medical School, Chicago, Illinois.
- Source
- Eur Heart J, 1988 Mar, 9 Suppl D:, 9-53
- Abstract
- The scientific foundations for risk factor modification in the elderly are
three-fold: (1) data from long-term prospective population studies demonstrating
significant independent relationships between established major risk
factors--particularly blood pressure (systolic and diastolic), serum
cholesterol, cigarette use, clinical diabetes--and risk of cardiovascular (CV)
morbidity and mortality; (2) data from population studies on time trends of mass
changes in major risk factors and parallel changes in CV mortality rates,
including large sustained declines; (3) data from randomized controlled trials
(RCTs). RCTs, the focus of this presentation, have been both unifactorial and
multifactorial. The former include several trials of antihypertensive drug
treatment, and of diet or drugs to lower serum cholesterol. When each of these
two sets of unifactorial trials is considered in its totality, the positive
nature of the findings is apparent. Among the antihypertensive drug trials,
two--the Hypertension Detection and Follow-up Program in the U.S.A. and the
study by the European Working Party on High Blood Pressure in the
Elderly--involved older men and women, both with significantly favourable
outcomes for their intensive treatment groups. Among the several trials on serum
cholesterol reduction, the Los Angeles Veterans Administration domiciliary study
involved elderly men, and showed significant reductions in incidence and
mortality from atherosclerotic events in its fat-modified diet group.
Multifactorial trials have involved middle-aged men. Their findings are
generally positive, particularly in regard to efficacy of life-style
interventions to modify diet and smoking habits. Degree of efficacy is
apparently related to degree of net change in risk factors in the intervention
group compared to the control group. All these findings lend strong support to
the judgment that risk factor modification, in the elderly as well as at younger
ages, is useful for the prevention of the major adult CV diseases and for
increasing longevity with health.
- Language of Publication
- English
- Unique Identifier
- 88242636
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document
- MeSH Heading (Major)
- Cardiovascular Diseases|MO/*PC
- MeSH Heading
- Adult; Age Factors; Aged; Blood Pressure; Cholesterol|BL; Clinical Trials;
Diet|AE; Female; Human; Hypercholesterolemia|DT; Hypertension|DT; Life Style;
Male; Middle Age; Risk Factors; Smoking; Support, Non-U.S. Gov't; Support, U.S.
Gov't, P.H.S.
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0195-668X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 30 from database: MEDLINE
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- Title
- Apolipoprotein E: cholesterol transport protein with expanding role in cell
biology.
- Author
- Mahley RW
- Address
- Gladstone Foundation Laboratories for Cardiovascular Disease, University of
California, San Francisco 94140-0608.
- Source
- Science, 1988 Apr 29, 240:4852, 622-30
- Abstract
- Apolipoprotein E is a plasma protein that serves as a ligand for low density
lipoprotein receptors and, through its interaction with these receptors,
participates in the transport of cholesterol and other lipids among various
cells of the body. A mutant form of apolipoprotein E that is defective in
binding to low density lipoprotein receptors is associated with familial type
III hyperlipoproteinemia, a genetic disorder characterized by elevated plasma
cholesterol levels and accelerated coronary artery disease. Apolipoprotein E is
synthesized in various organs, including liver, brain, spleen, and kidney, and
is present in high concentrations in interstitial fluid, where it appears to
participate in cholesterol redistribution from cells with excess cholesterol to
those requiring cholesterol. Apolipo-protein E also appears to be involved in
the repair response to tissue injury; for example, markedly increased amounts of
apolipoprotein E are found at sites of peripheral nerve injury and regeneration.
Other functions of apolipoprotein E, unrelated to lipid transport, are becoming
known, including immunoregulation and modulation of cell growth and
differentiation.
- Language of Publication
- English
- Unique Identifier
- 88204890
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document
- MeSH Heading (Major)
- Apolipoproteins E|GE/*PH; Cholesterol|*ME
- MeSH Heading
- Amino Acid Sequence; Biological Transport; Gene Expression Regulation;
Human; Hyperlipoproteinemia Type III|GE/ME; Immunity; Lipids|ME; Molecular
Sequence Data; Polymorphism (Genetics); Protein Conformation; Receptors, LDL|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0036-8075
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins E); 0 (Receptors, LDL); 57-88-5 (Cholesterol)
Record 31 from database: MEDLINE
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- Title
- Effects of calcium antagonists and adrenergic antihypertensive drugs on
plasma lipids and cellular cholesterol metabolism.
- Author
- Krone W; Müller-Wieland D; Nägele H; Behnke B; Greten H
- Address
- Medizinische Kerklinik und Poliklinik, Universitäts-Krankenhaus Eppendorf,
Hamburg, F.R.G.
- Source
- J Cardiovasc Pharmacol, 1987, 10 Suppl 10:, S199-202
- Abstract
- Calcium antagonists and antihypertensive alpha-adrenergic and
beta-adrenergic drugs may cause changes in plasma lipoprotein levels. Different
mechanisms by which these antihypertensive agents effect cellular lipid
metabolism have been proposed. The activity of lipoprotein lipase that
determines the catabolism of very low density lipoproteins (VLDL) is decreased
by the beta-blocker propranolol and increased by alpha 1-antagonists. The plasma
cholesterol or low density lipoprotein (LDL) level is inversely associated with
the number of LDL receptors. Catecholamines suppress the LDL receptor activity,
thus leading to an increase in plasma cholesterol concentration. The calcium
antagonist verapamil and the beta-blocker propranolol may increase LDL receptor
activity either per se or by its antagonizing effect on the catecholamine
action. The metabolism of high density lipoproteins (HDL) may be affected
directly by catecholamines, which might increase HDL binding activity, thereby
enhancing efflux of cholesterol from cells. Catecholamines inhibit cholesterol
biosynthesis in extrahepatic cells. The effects are mediated by alpha 2- and
beta 2-adrenergic receptors. Accordingly, the alpha 2-agonists clonidine and
alpha-methyldopa mimicked and propranolol opposed the catecholamine action. In
contrast, the alpha 1 antagonists indoramin, prazosin, and urapidil had no
effect on cholesterol synthesis. The results provide evidence that calcium
antagonists and various antihypertensive drugs, depending upon their action on
beta- or alpha-adrenergic receptors, affect lipid metabolism differently. The
metabolic effect may play a role in atherogenesis and may be of clinical
importance when antihypertensive treatment is considered.
- Language of Publication
- English
- Unique Identifier
- 88260207
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document
- MeSH Heading (Major)
- Antihypertensive Agents|*PD; Calcium Channel Blockers|*PD; Cholesterol|*ME;
Lipids|*BL
- MeSH Heading
- Adrenergic alpha-Antagonists|PD; Adrenergic beta-Antagonists|PD; Human;
Lipoproteins, HDL|ME; Lipoproteins, LDL Cholesterol|ME; Lipoproteins, VLDL|ME;
Liver|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0160-2446
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Adrenergic alpha-Antagonists); 0 (Adrenergic beta-Antagonists); 0
(Antihypertensive Agents); 0 (Calcium Channel Blockers); 0 (Lipoproteins, HDL);
0 (Lipoproteins, LDL Cholesterol); 0 (Lipoproteins, VLDL); 57-88-5 (Cholesterol)
Record 32 from database: MEDLINE
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- Title
- Role of macrophages in lipid metabolism.
- Author
- Kottke BA
- Address
- Atherosclerosis Research Unit, Mayo Clinic, Rochester, Minnesota 55905.
- Source
- J Cardiovasc Pharmacol, 1987, 10 Suppl 9:, S7-10
- Abstract
- One of the cells involved in lipid metabolism and thought to have adrenergic
receptors is the macrophage. Low-density lipoprotein (LDL), once modified, can
bind to modified LDL receptors on the macrophage. After binding to these
receptors, LDL is internalized by a mechanism that is not controlled by feedback
inhibition. This unregulated uptake results in massive cholesterol ester
accumulation in atherosclerotic plaques. Macrophages secrete apolipoprotein E, a
process that appears to be regulated by the cholesterol content of the
macrophage, as well as by lipoprotein lipase. Macrophages are also thought to
have receptors for high-density lipoprotein (HDL) on their surface, receptors
that may play a key role in reverse cholesterol transport of cholesterol esters
from the cells. Studies are being conducted to determine the effects of alpha
1-adrenergic activation on lipoprotein metabolism in these cells.
- Language of Publication
- English
- Unique Identifier
- 88092697
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document
- MeSH Heading (Major)
- Lipids|*ME; Macrophages|*ME
- MeSH Heading
- Animal; Apolipoproteins|ME; Cholesterol|ME; Endothelium|ME; Human;
Lipoproteins|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0160-2446
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins); 0 (Lipoproteins); 57-88-5 (Cholesterol)
Record 33 from database: MEDLINE
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- Title
- An epidemiologic appraisal of the associations between the fatty acids
esterifying serum cholesterol and some cardiovascular risk factors in
middle-aged men.
- Author
- Cambien F; Warnet JM; Vernier V; Ducimetière P; Jacqueson A; Flament C;
Orssaud G; Richard JL; Claude JR
- Address
- Unité d'Epidemiologie Cardiovasculaire, Institut National de la Santé et de
la Recherche Médicale, Paris, France.
- Source
- Am J Epidemiol, 1988 Jan, 127:1, 75-86
- Abstract
- The relations between the fatty acids of cholesterol esters and some
cardiovascular risk factors have been investigated in a sample of 3,348
middle-aged men examined at entry into the Paris Prospective Study 2. The
partial associations between the risk factors and the various fatty acids have
been evaluated using a special regression method that takes into account the
structural dependencies among the percentages of fatty acids. The results show
that palmitoleic acid is strongly associated with alcohol consumption and blood
pressure and that its association with blood pressure is absent in nondrinkers.
High density lipoprotein cholesterol and apolipoprotein A1 are negatively
associated with palmitic and dihomogammalinolenic acids and positively
associated with oleic and linoleic acids. An inverse relation of low density
lipoprotein cholesterol and apolipoprotein B to these fatty acids is also
observed. Simultaneous high levels of palmitic and dihomogammalinolenic acids
and low levels of oleic and linoleic acids could then be related to profiles of
lipids and apolipoproteins exposing one to a high risk of coronary heart
disease. These associations may be of interest in interpreting the relations
observed in other studies between the fatty acid composition of cholesterol
esters or other lipids and coronary heart disease.
- Language of Publication
- English
- Unique Identifier
- 88103499
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Cholesterol Esters|*BL; Coronary Disease|BL/*EP; Fatty
Acids|*BL
- MeSH Heading
- Blood Pressure; Epidemiologic Methods; Human; Male; Methods; Middle Age;
Models, Biological; Paris; Prospective Studies; Regression Analysis; Risk
Factors; Support, Non-U.S. Gov't; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW LITERATURE
- ISSN
- 0002-9262
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol Esters); 0 (Fatty Acids); 0 (Triglycerides); 57-88-5
(Cholesterol)
Record 34 from database: MEDLINE
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- Title
- Cholesteryl ester storage disease. Report of a case.
- Author
- Coelho CA; Balarin MA; Coelho KI
- Address
- Department of Pediatrics, School of Medicine, Paulista State University
(UNESP), Botucatu, SP.
- Source
- Arq Gastroenterol, 1987 Jul-Dec, 24:3-4, 184-7
- Abstract
- Cholesteryl ester storage disease (CESD) is a rare disorder of familial
incidence characterized by the accumulation of cholesteryl ester and
triglycerides in the liver, intestine and bone marrow. Until now only 21 cases
have been reported in the literature. We present a 9 months old girl presenting
with increased abdominal girth. She had normal liver function tests and
increased cholesterol and triglycerides serum levels. The liver biopsy showed
many cholesterol cristals seen as needle shaped cristals under polarized light.
This is the youngest patient being diagnosed clinically in the literature.
- Language of Publication
- English
- Unique Identifier
- 89087335
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document
- MeSH Heading (Major)
- Cholesterol Ester Storage Disease|BL/*DI/EP; Liver Diseases|BL/*DI/EP
- MeSH Heading
- Case Report; Cholesterol|BL; Female; Hepatomegaly|ET; Human; Infant;
Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES
- ISSN
- 0004-2803
- Country of Publication
- BRAZIL
- CAS Registry/EC Number
- 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 35 from database: MEDLINE
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- Title
- Enzymes involved in plasma cholesterol transport.
- Author
- Barter PJ; Hopkins GJ; Rajaram OV
- Address
-
- Source
- Baillieres Clin Endocrinol Metab, 1987 Aug, 1:3, 623-38
- Abstract
- Regulation of plasma cholesterol transport is to a large extent a function
of factors that regulate plasma cholesterol esterification and the transfers of
cholesteryl esters between plasma lipoprotein fractions. Plasma cholesterol
esterification is catalysed by the action of lecithin: cholesterol
acyltransferase on lipids on the surface of HDL, while the transfers of
cholesteryl esters require activity of a specific lipid transfer protein.
Esterification of the cholesterol on the surface of HDL generates a
concentration gradient down which unesterified cholesterol moves from tissues
into the plasma. Once within the plasma and esterified, the newly formed
cholesteryl esters are incorporated initially into the core of HDL particles
before being redistributed to other classes of lipoproteins. The end result of
these processes of esterification and transfer is that most of the cholesterol
in human plasma is accommodated within the core of LDL, where its transport is a
function of the highly regulated uptake by tissues of intact LDL particles. The
capacity of HDL to act as substrates for lecithin: cholesterol acyltransferase
varies inversely with HDL particle size. Thus, factors such as the concentration
of triglyceride-rich lipoproteins and activities of the lipid transfer protein,
hepatic lipase, lipoprotein lipase and the HDL conversion protein, which are
known to influence HDL particle size, may also be important as regulators of
plasma cholesterol esterification.
- Language of Publication
- English
- Unique Identifier
- 88240214
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Lecithin Acyltransferase|*ME; Lipoprotein Lipase|*ME
- MeSH Heading
- Animal; Cholesterol Esters|ME; Human; Lecithin Acyltransferase
Deficiency|BL; Models, Biological
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0950-351X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- EC 2.3.1.43 (Lecithin Acyltransferase); EC 3.1.1.34 (Lipoprotein Lipase); 0
(Cholesterol Esters); 57-88-5 (Cholesterol)
Record 36 from database: MEDLINE
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- Title
- Lipoproteins and atherosclerosis.
- Author
- Babiak J; Rudel LL
- Address
-
- Source
- Baillieres Clin Endocrinol Metab, 1987 Aug, 1:3, 515-50
- Abstract
- The plasma lipoproteins are the primary means of transport of cholesterol
among tissues. In particular, the apo B-containing lipoproteins (VLDL, IDL and
LDL) are important for the delivery of cholesterol from the liver to peripheral
tissues, while HDL appear to mediate the reverse process of movement of
cholesterol from tissues back to the liver. Both of these transport processes
are necessary for efficient whole body cholesterol homeostasis, because the
liver is the major site of both the production and excretion of cholesterol.
However, deviations from a proper balance of transport of cholesterol, either
increases in LDL levels or decreases in HDL cholesterol flux, may result in
accumulation of cholesterol in extrahepatic tissues. Increased risk of
atherosclerosis and CHD may be associated with elevation in the number of LDL
particles, increase or decrease in LDL particle size, or changes in the
composition of plasma LDL. These modifications of plasma LDL may be brought
about following perturbation of one of several aspects of LDL metabolism. These
include decreased LDL receptor activity, increased VLDL production and
cholesterol enrichment of the liver-derived VLDL. The events in the arterial
wall that make some LDL particles apparently atherogenic are not well
understood. In the case of nonhuman primates, large-size LDL are associated with
an increased risk of CHD. One characteristic of these LDL is that their core
lipids are rich in saturated cholesteryl esters and their transition
temperatures are frequently above body temperature. The liquid crystalline
cholesteryl ester cores of such LDL may modulate the conformation of apo B on
the surface and thereby affect the interaction of these LDL with cellular
receptors or connective tissue matrix proteoglycans. It is likely, though, that
changes in LDL particle number, LDL particle size and LDL particle composition
may each contribute to progression of atherosclerosis. The presumed metabolic
events that make HDL protective against atherosclerosis have been termed reverse
cholesterol transport, and suggest that small HDL that are deficient in free
cholesterol acquire this lipid from cell membranes. The HDL cholesterol is
esterified by LCAT in the circulation, forming large HDL that can then deliver
the cholesteryl ester to the liver by both direct and indirect means. In most
circumstances, it is assumed that an increase in plasma HDL cholesterol
concentration reflects an increase in the rate at which HDL is removing
cholesterol from tissues and, consequently, a decrease in
atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
- Language of Publication
- English
- Unique Identifier
- 88240210
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document
- MeSH Heading (Major)
- Arteriosclerosis|*ET; Atherosclerosis|*ET; Lipoproteins|BL/*PH
- MeSH Heading
- Apolipoproteins B|PH; Biological Transport; Cholesterol|ME; Coronary
Disease|ET; Endothelium, Vascular|ME; Human; Lipoproteins, HDL|BL/PH;
Lipoproteins, LDL|BL/PH; Lipoproteins, VLDL|BL/PH; Macrophages|ME; Models,
Biological; Risk Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0950-351X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Apolipoproteins B); 0 (Lipoproteins); 0 (Lipoproteins, HDL); 0
(Lipoproteins, VLDL); 57-88-5 (Cholesterol)
Record 37 from database: MEDLINE
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- Title
- Lipid transport through the plasma: the metabolic basis of hyperlipidaemia.
- Author
- Shepherd J; Packard CJ
- Address
-
- Source
- Baillieres Clin Endocrinol Metab, 1987 Aug, 1:3, 495-514
- Abstract
- Plasma lipid abnormalities derive their importance from their association
with coronary artery disease. Elevated cholesterol levels accentuate risk, and
clinical trials have shown that reductions lead to a decline in coronary events.
The major plasma lipids, cholesterol and triglyceride, circulate in association
with specific proteins as lipid-protein or lipoprotein complexes. The proteins
direct and regulate the metabolism of these complexes by interacting with tissue
enzymes and receptors. The metabolic fate of circulating triglyceride is
governed by the activity of the enzyme lipoprotein lipase, situated in adipose
tissue and skeletal muscle. Cellular demand for cholesterol, on the other hand,
is met by activation of a specific receptor which mediates the delivery of
sterol-rich lipoproteins to lysosomal degradation in liver and peripheral
tissues. In order to prevent excess cholesterol accumulation at the periphery,
there is a system of reverse cholesterol transport which involves assimilation
and trapping of the sterol in the plasma lipoproteins through the action of the
enzyme lecithin:cholesterol acyltransferase. Thereafter, the cholesterol is
delivered to the liver, the only organ capable of excreting it in significant
amounts. Disturbances in these processes may produce gross changes in the plasma
lipid profile, clearly recognizable as hyperlipidaemia. However, it is becoming
increasingly clear that a number of inherited traits can subtly perturb the
lipoprotein spectrum and increase coronary risk even in subjects whose plasma
lipoprotein profile would be considered normal.
- Language of Publication
- English
- Unique Identifier
- 88240208
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document
- MeSH Heading (Major)
- Hyperlipidemia|*BL; Lipids|*BL
- MeSH Heading
- Apolipoproteins|BL; Biological Transport, Active; Cholesterol|BL; Dietary
Fats|ME; Human; Lipoproteins|BL; Liver|ME; Models, Biological; Support, Non-U.S.
Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0950-351X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Apolipoproteins); 0 (Dietary Fats); 0 (Lipoproteins); 57-88-5
(Cholesterol)
Record 38 from database: MEDLINE
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- Title
- Hypo- and hyperresponders: individual differences in the response of serum
cholesterol concentration to changes in diet.
- Author
- Beynen AC; Katan MB; Van Zutphen LF
- Address
- Department of Laboratory Animal Science, State University, Utrecht, The
Netherlands.
- Source
- Adv Lipid Res, 1987, 22:, 115-71
- Abstract
- The feeding of cholesterol-rich diets to random-bred animals results in
marked interindividual differences in the response of serum cholesterol. Certain
animals show only small responses (hyporesponders), whereas others develop high
degrees of hypercholesterolemia (hyperresponders). Inbred strains of rabbits,
rats, and mice differing in their sensitivity to dietary cholesterol are
available. In these animals, and also in monkeys, the responsiveness to
high-cholesterol diets has a strong genetic basis. The existence of hyper- and
hyporesponders also holds in humans, though not as pronounced as in laboratory
animals. Repeated trials with the same subjects have shown that persons exist
with a consistently low or high response to increased intakes of cholesterol.
However, "spontaneous," diet-independent within-person variations in
the level of serum cholesterol markedly inflate the between-person variation in
the response of serum cholesterol; both variations are of the same order of
magnitude. Hypo- and hyperresponsiveness to dietary cholesterol extends to other
hypercholesterolemic components of the diet. In humans and rabbits
hyperresponsiveness to dietary cholesterol is associated with responsiveness to
dietary saturated fatty acids. The mechanisms underlying hypo- and
hyperresponsiveness to dietary cholesterol have not yet been unraveled. On the
basis of available data, we propose that in hyperresponders, compared with
hyporesponders, there is a higher hepatic efflux of cholesterol in low-density
lipoproteins (LDL), or its precursors, after cholesterol consumption. This may
be caused by insufficient inhibition of cholesterol biosynthesis and/or the high
capacity of cholesterol absorption in the hyperresponders. The stimulation of
LDL production accounts for the increase in LDL cholesterol in serum. The number
of hepatic LDL receptors, which may be already decreased in hyperresponders,
will decrease further through down-regulation. The receptor-mediated LDL
clearance decreases, but the absolute amount of LDL cholesterol taken up by the
cells via the receptor and by the receptor-independent pathway increases because
of the increased level of LDL cholesterol. In this way a new equilibrium is
reached in which LDL production equals LDL catabolism. The phenomenon of hypo-
and hyperresponsiveness may have implications for counseling subjects who
attempt to lower their serum cholesterol by diet. However, identification of
true hyper- and hyporesponders is greatly hampered by within-person fluctuations
of the level of serum cholesterol. No simple test is available to discriminate
hypo- from hyperresponders.(ABSTRACT TRUNCATED AT 400 WORDS)
- Language of Publication
- English
- Unique Identifier
- 88180512
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document
- MeSH Heading (Major)
- Cholesterol|*BL/PK; Cholesterol, Dietary|AD/*AE;
Hypercholesterolemia|BL/*ET/GE
- MeSH Heading
- Animal; Comparative Study; Human; Lipoproteins|BL; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0065-2849
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol, Dietary); 0 (Lipoproteins); 57-88-5 (Cholesterol)
Record 39 from database: MEDLINE
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- Title
- Lovastatin: a new cholesterol-lowering agent.
- Author
- Krukemyer JJ; Talbert RL
- Address
- College of Pharmacy, Columbus, Ohio.
- Source
- Pharmacotherapy, 1987, 7:6, 198-210
- Abstract
- Lovastatin is a potent new drug for lowering serum cholesterol through
inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting
enzyme for cholesterol biosynthesis. Metabolic studies with lovastatin in
healthy volunteers and patients with hypercholesterolemia suggest reduced
synthesis of low-density lipoprotein cholesterol (LDL-C) as well as enhanced
catabolism LDL-C mediated through LDL receptors as the principal mechanisms for
lipid-lowering effects. Total cholesterol and LDL-C are reduced by 30% or more
on average when added to baseline therapy, with the effects being more
pronounced in nonfamilial than in familial hypercholesterolemia. Optimal dosing
appears to be 20 mg given twice a day. The most common adverse effects are
gastrointestinal, while the most serious are elevated transaminase levels and
the potential for lens opacities. Lovastatin is the first of a new class of
lipid-lowering agents, and is effective when added to diet therapy or in
combination with other drugs.
- Language of Publication
- English
- Unique Identifier
- 88176566
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Lovastatin|PD/*TU
- MeSH Heading
- Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0277-0008
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol); 75330-75-5 (Lovastatin)
Record 40 from database: MEDLINE
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- Title
- Plasma cholesterol variation in the National Heart, Lung and Blood Institute
Twin Study.
- Author
- Christian JC; Borhani NO; Castelli WP; Fabsitz R; Norton JA Jr; Reed T;
Rosenman R; Wood PD; Yu PL
- Address
- Department of Medical Genetics, Indiana University School of Medicine,
Indianapolis 46223.
- Source
- Genet Epidemiol, 1987, 4:6, 433-46
- Abstract
- Plasma cholesterol was measured in the fifth decade of the life of 249 pairs
of monozygotic (MZ) and 262 pairs of dizygotic (DZ) World War II veteran twins
and 70% of the same cohort 10 years later. There were no significant differences
between the mean cholesterol values for MZ and DZ twins, and the within DZ pair
mean squares were significantly larger than the within MZ pair mean squares for
all of the cholesterol variables measured. However, the DZ twins were found to
have greater total variance, positive skewness, and leptokurtosis than the MZ
twins for total and high-density lipoprotein cholesterol, and the
total/high-density ratio. Comparisons with published data revealed that the
variance of DZ twins was similar to that of singletons while the MZ twins have
smaller total variance, perhaps owing to a missing component of variation.
Hypotheses for the source of the differences in the zygosity distributions are
proposed including environmental influences (pre- or post-natal and within- or
among-families), genetic differences, and selection at the time of induction
into the armed services. Because of the differences in total variance of the two
zygosities it is difficult to know which estimates of genetic variance or
heritability have the least bias. However, these data provide clues that may
lead to further understanding of sources of plasma cholesterol variation that
could be important to the future understanding of risk for coronary heart
disease.
- Language of Publication
- English
- Unique Identifier
- 88112744
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Lipoproteins, HDL Cholesterol|*BL; Twins|*; Twins,
Dizygotic|*; Twins, Monozygotic|*
- MeSH Heading
- Human; Longitudinal Studies; Male; Support, U.S. Gov't, P.H.S.; United
States; United States Public Health Service; Variation (Genetics)
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES
- ISSN
- 0741-0395
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 57-88-5 (Cholesterol)
Record 41 from database: MEDLINE
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- Title
- Total cholesterol and high density lipoprotein cholesterol levels in
populations differing in fat and carbohydrate intake.
- Author
- Knuiman JT; West CE; Katan MB; Hautvast JG
- Address
- Department of Human Nutrition, Agricultural University, Wageningen, The
Netherlands.
- Source
- Arteriosclerosis, 1987 Nov-Dec, 7:6, 612-9
- Abstract
- This paper reviews epidemiological studies on the relationship between diet
and high density lipoproteins (HDL), with emphasis on the authors' studies of
boys and men from different countries and with different dietary habits. Sera
were collected from boys (ages 7 to 9 years) and men (ages 33 to 48 years) in 20
countries, and these were analyzed in one standardized laboratory. In boys,
total and HDL cholesterol changed in parallel, from low values in populations in
developing countries with low-fat, high-carbohydrate diets to high values in
affluent populations. The correlation between HDL and total cholesterol was 0.90
(n = 16 populations). A similar trend was seen in groups of vegetarian and
omnivorous boys within one region. Detailed analyses of individual diets of boys
in five countries showed a negative relation between carbohydrate intake and HDL
cholesterol both for group means (r = -0.99, n = 5) and for individual boys
within one country (r = -0.26 to 0.04, n = 109 to 133 boys per country). In
these boys, differences in obesity and physical activity were slight, and
unrelated to differences in HDL. Total cholesterol rose with saturated fat
intake (r = 0.87 for five population means; r = 0.07 to 0.26 within population
groups). In adult men, total and HDL cholesterol also tended to rise
simultaneously with affluence. However, the relation was much weaker (r = 0.60,
n = 13 population groups).(ABSTRACT TRUNCATED AT 250 WORDS)
- Language of Publication
- English
- Unique Identifier
- 88076534
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Diet|*; Dietary Carbohydrates|*AD; Dietary Fats|*AD;
Lipoproteins, HDL|*BL
- MeSH Heading
- Adult; Africa; Asia; Child; Comparative Study; Europe; Human; Male; Middle
Age; Obesity|BL; Support, Non-U.S. Gov't; United States; Vegetarianism
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0276-5047
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Dietary Fats); 0 (Lipoproteins, HDL); 57-88-5 (Cholesterol)
Record 42 from database: MEDLINE
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- Title
- Fibric acids: effects on lipids and lipoprotein metabolism.
- Author
- Grundy SM; Vega GL
- Address
- University of Texas Health Science Center, Center for Human Nutrition,
Dallas 75235-9052.
- Source
- Am J Med, 1987 Nov 27, 83:5B, 9-20
- Abstract
- The major effect of the fibrates on triglycerides is to promote
triglyceride-rich lipoprotein catabolism through increased lipoprotein lipase
activity. Fibrates also enhance lipolysis of plasma triglycerides by a means
different from that of caloric restriction. Their effect on very low-density
lipoprotein metabolism also differs from that of nicotinic acid. The effect of
fibrate therapy upon low-density lipoprotein-cholesterol concentrations depends
upon the patients' overall lipoprotein status. The responsible mechanisms are
not understood. In hypertriglyceridemic patients, fibrates often reverse
abnormal changes in low-density lipoprotein composition; low-density lipoprotein
heterogeneity is reduced and small dense low-density lipoproteins are
eliminated, apparently secondary to reduced levels of triglyceride-rich
lipoproteins. Kinetic studies indicate that fibrates do not enhance low-density
lipoprotein formation rates, thus contradicting the idea that fibrate therapy
causes increased low-density lipoprotein cholesterol levels via increased
conversion of very low-density lipoprotein to low-density lipoprotein. Though
enhanced low-density lipoprotein catabolism in hypertriglyceridemia could occur
via several mechanisms, the responsible factors are largely reversed by fibrate
therapy. In non-hypertriglyceridemic patients, fibrates may actually enhance the
fractional clearance of low-density lipoprotein and thus reduce low-density
lipoprotein levels. Fibrate therapy reverses the typical high-density
lipoprotein pattern of hypertriglyceridemic patients, producing more
high-density lipoprotein2a and less high-density lipoprotein2b. Such treatment
also increases high-density lipoprotein cholesterol levels in patients without
definite hypertriglyceridemia. Synthesis rates of apolipoproteins AI and AII may
be affected by fibrates. The fibrates' major effects on sterol metabolism are
interference with cholesterol and bile acid synthesis and increased cholesterol
secretion into bile. Although bile saturation increases in most patients, in
only a relatively small percentage do gallstones actually develop;
super-saturated bile is not sufficient to induce gallstone formation in most
patients. Available data strongly imply that fibrates mobilized cholesterol out
of tissue pools, perhaps by altering tissue cell membranes to allow cholesterol
release from the cell surfaces.
- Language of Publication
- English
- Unique Identifier
- 88074443
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document
- MeSH Heading (Major)
- Clofibrate|*AA/PD; Triglycerides|*ME
- MeSH Heading
- Antilipemic Agents|PD; Bezafibrate|PD; Bile Acids and Salts|BI;
Cholesterol|BI; Human; Lipoproteins, HDL|ME; Lipoproteins, LDL|BI/ME;
Lipoproteins, VLDL|BI; Liver|ME; Pentanoic Acids|PD; Procetofen|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9343
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antilipemic Agents); 0 (Bile Acids and Salts); 0 (Lipoproteins, HDL); 0
(Lipoproteins, VLDL); 0 (Pentanoic Acids); 0 (Triglycerides); 25812-30-0
(Gemfibrozil); 41859-67-0 (Bezafibrate); 49562-28-9 (Procetofen); 57-88-5
(Cholesterol); 637-07-0 (Clofibrate)
Record 43 from database: MEDLINE
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- Title
- Structure and biochemical effects of fenofibrate.
- Author
- Kloer HU
- Address
- Department of Medicine, University of Giessen, Federal Republic of Germany.
- Source
- Am J Med, 1987 Nov 27, 83:5B, 3-8
- Abstract
- The structures of various fibric acid derivatives are compared. Fenofibrate
inhibits de novo hepatic fatty acid synthesis and seems to inhibit hepatic very
low-density lipoprotein synthesis, but it enhances mitochondrial and peroxisomal
fatty acid oxidation and lipoprotein lipase activity. It produces a very
significant reduction in the plasma triglyceride concentration. Fenofibrate also
inhibits cholesterol synthesis prior to processing mevalonate, indirectly
causing significant reduction of hydroxymethylglutaryl coenzyme A reductase
activity. The drug may inhibit acyl-coenzyme A-cholesterol transferase activity,
reducing cholesterol ester accumulation within cells. Fenofibrate significantly
increases the fractional rate of lecithin-cholesterol acyltransferase activity
in normolipidemic and hypercholesterolemic patients. This may explain the
increase in cholesterol ester levels observed in high-density lipoproteins. It
may stimulate bile acid synthesis from exogenous cholesterol. It causes a marked
reduction of increased spontaneous platelet aggregation. Fenofibrate also
markedly diminishes the effect of platelet-derived growth factor upon DNA
synthesis in vitro, an effect that might impede a key event in early
atherogenesis. Thus, fenofibrate has effects not directly related to its lipid-
and lipoprotein-lowering action.
- Language of Publication
- English
- Unique Identifier
- 88074434
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document
- MeSH Heading (Major)
- Fatty Acids|*BI; Procetofen|*PD; Propionates|*PD; Triglycerides|*ME
- MeSH Heading
- Chemistry; Cholesterol|BI/ME; DNA|BI; Human; Lecithin Acyltransferase|ME;
Platelet Aggregation|DE; Platelet-Derived Growth Factor|AI
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9343
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 2.3.1.43 (Lecithin Acyltransferase); 0 (Fatty Acids); 0 (Platelet-Derived
Growth Factor); 0 (Propionates); 0 (Triglycerides); 49562-28-9 (Procetofen);
57-88-5 (Cholesterol); 9007-49-2 (DNA)
Record 44 from database: MEDLINE
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- Title
- The role of linoleic acid and its metabolites in the lowering of plasma
cholesterol and the prevention of cardiovascular disease.
- Author
- Horrobin DF; Huang YS
- Address
- Efamol Research Institute, Kentville, Nova Scotia, Canada.
- Source
- Int J Cardiol, 1987 Dec, 17:3, 241-55
- Abstract
- An increase in linoleic acid intake lowers plasma cholesterol and is one of
the safest methods for achieving this end. However, the amounts that must be
consumed are large. Linoleic acid is metabolized via several routes and it is
probable that a metabolite, rather than linoleic acid itself, is responsible for
the cholesterol-lowering effect. If that metabolite could be identified, safe,
drug-free, cholesterol-lowering might be achieved with much lower doses.
Evidence is reviewed which suggests that a long-chain polyunsaturated fatty acid
and/or a prostaglandin metabolite may be responsible for the
cholesterol-controlling action of linoleic acid. Such metabolites may be
effective also in controlling other risk factors for cardiovascular disease,
such as elevated blood pressure and enhanced platelet aggregation.
Epidemiological studies suggest that low levels of those metabolites, especially
dihomogammalinolenic acid and arachidonic acid, are powerful independent risk
factors for development of ischaemic heart disease. Further research in this
area is urgently needed now that it is broadly accepted that
cholesterol-lowering does indeed reduce the risk of cardiovascular disease.
- Language of Publication
- English
- Unique Identifier
- 88057739
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document
- MeSH Heading (Major)
- Cardiovascular Diseases|*PC; Cholesterol|*BL; Linoleic Acids|*PH
- MeSH Heading
- Human; Risk Factors; Structure-Activity Relationship
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0167-5273
- Country of Publication
- NETHERLANDS
- CAS Registry/EC Number
- 0 (Linoleic Acids); 57-88-5 (Cholesterol)
Record 45 from database: MEDLINE
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- Title
- The use of diet to lower plasma cholesterol levels.
- Author
- Riccardi G; Rivellese AA; Mancini M
- Address
- Institute of Internal Medicine and Metabolic Diseases, 2nd Medical School,
University of Naples, Italy.
- Source
- Eur Heart J, 1987 Aug, 8 Suppl E:, 79-85
- Abstract
- The basic principle of a lipid lowering diet is restriction of saturated fat
intake. This can be achieved by reducing the consumption of dairy products and
fats of animal origin. To keep energy intake constant (in normal weight
individuals) complex carbohydrate or unsaturated fat is substituted for
saturated fat. Diets with various proportions of complex carbohydrate,
monounsaturated fatty acids, and polyunsaturated fatty acids have been proposed.
In theory, the latter should be the best substitute for saturated fatty acids in
a lipid lowering diet. Polyunsaturated fat has cholesterol lowering activity
that is additive to the effect obtained by reducing the amount of dietary
saturated fat. In practice, either polyunsaturated fatty acids or
monounsaturated fatty acids or complex carbohydrate exert very similar effects
on plasma cholesterol levels when substituted for saturated fatty acids in a
lipid lowering diet. Their effects on plasma triglyceride are, however,
dissimilar. Increased consumption of polyunsaturated fat leads to pronounced
reduction in plasma triglyceride concentrations. Conversely, a high carbohydrate
diet has a hypertriglyceridemic effect that is more pronounced in individuals
with diabetes or preexisting hypertriglyceridemia. Dietary cholesterol should
also be reduced in order to lower plasma cholesterol levels. However, the
hypocholesterolemic effect of this measure has a large interindividual variation
which is further influenced by the fat composition of the diet. Dietary fibre
has received attention in more recent years for its ability to reduce plasma
cholesterol levels. Fibre rich foods are not equally effective in this respect,
the most active being legumes, fruit and vegetables. When high carbohydrate-high
fibre diets are consumed, the hypertriglyceridaemic effect of carbohydrate is
counteracted by dietary fibre.(ABSTRACT TRUNCATED AT 250 WORDS)
- Language of Publication
- English
- Unique Identifier
- 88055129
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Diet|*
- MeSH Heading
- Coronary Disease|PC; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0195-668X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 46 from database: MEDLINE
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- Title
- Interpopulation correlations between serum cholesterol level and the
occurrence of coronary heart disease.
- Author
- Pyörälä K
- Address
- Department of Medicine, University of Kuopio, Finland.
- Source
- Eur Heart J, 1987 Aug, 8 Suppl E:, 23-30
- Abstract
- Epidemiological studies have established beyond any doubt that diet-related
differences in the population distributions for serum total cholesterol (low
density lipoprotein cholesterol) explain a large proportion of the
interpopulation variation in the occurrence of coronary heart disease (CHD).
These findings emphasize the central importance of appropriate dietary changes
in the prevention of CHD in populations with high population mean levels for
serum total cholesterol and high CHD rates. The possible contribution of
differences in the population distributions for serum high density lipoprotein
cholesterol to the interpopulation variation in the occurrence of CHD still
remains an unsolved issue.
- Language of Publication
- English
- Unique Identifier
- 88055120
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|BL/*EP; Population Surveillance|*
- MeSH Heading
- Diet|AE; Female; Human; Male; World Health
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE
- ISSN
- 0195-668X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 47 from database: MEDLINE
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- Title
- Coffee and cholesterol in epidemiological and experimental studies.
- Author
- Thelle DS; Heyden S; Fodor JG
- Address
- Institute of Community Medicine, Tromso, Norway.
- Source
- Atherosclerosis, 1987 Oct, 67:2-3, 97-103
- Abstract
- Twenty-two cross-sectional studies involving 130,000 persons from 8
different countries have reported their findings on the association between
coffee consumption and cholesterol levels. Results of these reports display a
variety of trends in the association between coffee intake and serum cholesterol
concentrations: 8 (36%) studies demonstrated a significant positive association
in both sexes, and 5 (23%) studies showed no association in men or women. In 3
other reports where both sexes were included, significant positive association
was observed only in women. The remaining 6 investigations examined only men
with 4 (18%) reporting a significant correlation between coffee and cholesterol.
This unexplained incongruity of cross-sectional data points to a relationship
between coffee and cholesterol in some populations, which needs to be further
explored. In addition, HDL cholesterol levels appeared unrelated to coffee
intake in the 11 studies in which it was measured. The 7 available human
experiments showed the same low level of agreement in the results among small
numbers of volunteers. Experiments involving different brewing methods suggest
that a major part of the cholesterol-increasing effect can be explained by
different brewing methods. A critical assessment of the published reports leads
to the conclusion that the data are insufficient to warrant public health
admonitions against coffee drinking, but that it may be of clinical importance
in some hypercholesterolemic individuals.
- Language of Publication
- English
- Unique Identifier
- 88049941
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coffee|*AE
- MeSH Heading
- Epidemiologic Methods; Female; Human; Male; Sex Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0021-9150
- Country of Publication
- NETHERLANDS
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 48 from database: MEDLINE
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- Title
- Plasma lipid concentrations: the concept of "normality" and its
implications for detection of high cardiovascular risk.
- Author
- Lewis B
- Address
- Department of Chemical Pathology and Metabolic Disorders, United Medical
School of St Thomas's Hospital, London.
- Source
- J Clin Pathol, 1987 Sep, 40:9, 1118-27
- Abstract
- The relation between serum cholesterol concentrations and the incidence of
coronary heart disease is continuous and curvilinear; there is neither
epidemiological nor biological evidence to support the existence of a threshold
value. There is a clinical need, however, for an acceptable definition of action
limits and desirable ranges, based on the evidence that raised cholesterol
concentrations are causally related to atherosclerotic heart disease. The
European Atherosclerosis Society has proposed a set of cut off points, which,
together with age and the presence of other risk factors, direct the clinician
to an appropriate level of treatment. Because the changes of serum cholesterol
during adult life appear unphysiological, these action limits do not require
adjustment for age. The distribution of serum cholesterol in the United Kingdom
population is such that a case finding strategy is required to identify the many
persons at very high risk of coronary disease. Measurements of triglyceride,
high density lipoprotein, apolipoproteins, and the investigation of
hyperlipoproteinemia are informative but less mandatory.
- Language of Publication
- English
- Unique Identifier
- 88033749
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|BL/*PC
- MeSH Heading
- Adult; Disease Susceptibility; Female; Human; Hyperlipidemia|PC;
Lipoproteins|BL; Male; Middle Age
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0021-9746
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Lipoproteins); 57-88-5 (Cholesterol)
Record 49 from database: MEDLINE
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- Title
- Cholesterol and myocardial membrane function.
- Author
- van der Laarse A
- Address
- Department of Cardiology, University Hospital Leiden, The Netherlands.
- Source
- Basic Res Cardiol, 1987, 82 Suppl 1:, 137-45
- Abstract
- The incorporation of cholesterol into phospholipid membranes changes the
physical properties of the membranes, such as their phase transition, fluidity
and homogeneity. In cholesterol-containing phospholipid membranes, integral
proteins are surrounded by "annular" phospholipids which exclude
cholesterol. Cellular cholesterol is supplied by circulating low-density
lipoproteins, and by intracellular de novo synthesis. Cholesterol removal is
predominantly handled by circulating high-density lipoproteins. In
cardiomyopathic hamsters, myocardial membranes (sarcolemma, mitochondria,
sarcoplasmic reticulum) have an increased cholesterol content. In ischaemic
myocardium, cholesterol content of sarcolemma fell and that of mitochondria
rose. Apparently, cholesterol is redistributed within the ischaemic heart cell.
Phospholipids are degraded in sarcolemma, mitochondria and sarcoplasmic
reticulum of ischaemic heart cells, probably by activation of phospholipases
present in these membrane systems.
- Language of Publication
- English
- Unique Identifier
- 88023781
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document
- MeSH Heading (Major)
- Cholesterol|*ME; Myocardium|*ME
- MeSH Heading
- Animal; Cell Membrane|ME; Coronary Disease|ME; Human; Membrane Lipids|ME;
Phospholipids|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0300-8428
- Country of Publication
- GERMANY, WEST
- CAS Registry/EC Number
- 0 (Membrane Lipids); 0 (Phospholipids); 57-88-5 (Cholesterol)
Record 50 from database: MEDLINE
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- Title
- Biliary cholesterol--friend or foe?
- Author
- Jacyna MR; Ross PE; Bouchier IA
- Address
- Department of Medicine, Ninewells Hospital and Medical School, Dundee,
Scotland.
- Source
- Q J Med, 1986 Nov, 61:235, 991-5
- Abstract
- It has hitherto been assumed that the cholesterol in bile simply represents
an excretory mechanism for cholesterol surplus to bodily requirements. However,
recent evidence suggests that this is not the case and that biliary cholesterol
has other functions. The functions consist of a mucosal protective effect
against the toxic action of bile-salts and also a role in regulating dietary
cholesterol absorption. Biliary cholesterol is clearly more than just an
excretory substance and serves other important physiological roles.
- Language of Publication
- English
- Unique Identifier
- 88016814
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document
- MeSH Heading (Major)
- Bile|ME/*PH; Cholesterol|ME/*PH
- MeSH Heading
- Human; Intestinal Mucosa|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0033-5622
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 51 from database: MEDLINE
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- Title
- Receptors in the regulation of lipoprotein metabolism.
- Author
- Packard CJ; Sheperd J
- Address
- University Department of Pathological Biochemistry, Royal Infirmary,
Glasgow.
- Source
- Ann Biol Clin (Paris), 1988, 46:1, 5-9
- Abstract
- Mamalian cholesterol metabolism is governed by two key features of the
steroid nucleus: it is poorly soluble in plasma and it cannot be degraded in
animal tissues. Cells which require the lipid import it through their
cytoplasmic membranes in the form of solubilized lipid-protein complexes, and a
similar export mechanism is essential in order to maintain cellular homeostasis.
The translocation is mediated by high affinity receptors which, under normal
circumstances, operate in close synchrony. Changes in the nature of the
lipoprotein ligand or the cell itself may disturb this balance and lead to the
pathological sterol accumulation which characterizes artherosclerosis lesions.
All body tissues engage in this traffic in cholesterol but the liver is the
single most important organ since it has the capacity both to synthesize large
quantities of the lipid and to excrete it from the body via a variety of
receptors designed to maintain peripheral sterol levels within safe limits.
- Language of Publication
- English
- Unique Identifier
- 88267587
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document
- MeSH Heading (Major)
- Lipoproteins|*ME; Receptors, Cell Surface|*PH
- MeSH Heading
- Cholesterol|ME; Human; Hypercholesterolemia, Familial|DT/ME;
Hyperlipoproteinemia Type III|DT/ME; Receptors, LDL|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0003-3898
- Country of Publication
- FRANCE
- CAS Registry/EC Number
- 0 (Lipoproteins); 0 (Receptors, Cell Surface); 0 (Receptors, LDL); 57-88-5
(Cholesterol)
Record 52 from database: MEDLINE
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- Title
- Cholesterol granuloma of the jaws. Report of a case.
- Author
- Hirshberg A; Dayan D; Buchner A; Freedman A
- Address
- Section of Oral Pathology and Oral Medicine, Maurice and Gabriela
Goldschleger School of Dental Medicine, Tel Aviv University, Israel.
- Source
- Int J Oral Maxillofac Surg, 1988 Aug, 17:4, 230-1
- Abstract
- A case of a cholesterol granuloma of the mandible, which manifested as a
solitary radiolucent lesion in an edentulous area, is presented. There is a lack
of accurate data regarding its nomenclature and pathogenesis. In this report,
the literature is reviewed, the nomenclature is clarified and the pathogenesis
discussed.
- Language of Publication
- English
- Unique Identifier
- 89010052
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document
- MeSH Heading (Major)
- Cholesterol|*; Granuloma|*PA; Mandibular Diseases|*PA
- MeSH Heading
- Case Report; Diagnosis, Differential; Female; Human; Jaw Cysts|PA; Middle
Age
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0901-5027
- Country of Publication
- DENMARK
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 53 from database: MEDLINE
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- Title
- Review of serum lipids and apolipoproteins in risk-assessment of coronary
heart disease.
- Author
- Rifai N; Chapman JF; Silverman LM; Gwynnes JT
- Address
- Department of Laboratory Medicine, Children's Hospital National Medical
Center, Washington, DC 20010.
- Source
- Ann Clin Lab Sci, 1988 Nov-Dec, 18:6, 429-39
- Abstract
- Coronary heart disease (CHD), the leading cause of death in the western
world, is multifactorial in nature. Abnormal lipoprotein levels are among the
risk factors that cause atherosclerosis and, therefore, have been used as
biochemical markers in assessing risk of developing CHD. The measurement of
serum cholesterol, lipoprotein cholesterol, and apolipoproteins accurately and
reliably has been hampered with technical difficulties. In addition, the
interpretation of these tests and the determination of their clinical values
have been challenging for both physicians and laboratory scientists. This
article addresses and reviews the major current analytical and clinical concerns
in the testing of lipids as well as the prevention and treatment of CHD.
- Language of Publication
- English
- Unique Identifier
- 89192172
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document
- MeSH Heading (Major)
- Apolipoproteins|*BL; Cholesterol|*BL; Coronary Disease|*BL
- MeSH Heading
- Adult; Female; Human; Male; Risk Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0091-7370
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins); 57-88-5 (Cholesterol)
Record 54 from database: MEDLINE
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- Title
- Lipids, clotting factors, and diabetes: endogenous risk factors for
cardiovascular disease.
- Author
- Lobo RA
- Address
- Department of Obstetrics and Gynecology, University of Southern California
School of Medicine, Los Angeles.
- Source
- Am J Obstet Gynecol, 1988 Jun, 158:6 Pt 2, 1584-91
- Abstract
- Theories of intimal injury leading to plaque formation include platelet
adhesion and production of growth factors, hypercholesterolemia, smooth muscle
cell proliferation, macrophage activity, defective utilization of low-density
lipoproteins via deficient receptors, and deficiency in cellular lysosomal
enzymes. High levels of low-density lipoproteins and intermediate-density
lipoproteins, as well as their apoproteins, are strong risk factors for
cardiovascular disease. The lowering of the cholesterol level has been shown to
produce significant regression of atherosclerotic lesions. Data also suggest an
interaction between lipids and platelets, although the role of coagulation
disorders as an independent risk factor for atherosclerosis is difficult to
assess. Although much of the data are controversial, there is evidence that
platelet survival time is a strong predictor of severe vessel damage. In
addition, some studies have reported decreased activity of antithrombin III with
coronary artery disease, and there appears to be a direct correlation between
fibrinogen and cholesterol levels. Finally, diabetes mellitus (both types I and
II) is a significant independent risk factor for atherosclerosis. The risk is
not related to the severity or duration of diabetes, and it appears to be
greater in women than in men.
- Language of Publication
- English
- Unique Identifier
- 88238700
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document
- MeSH Heading (Major)
- Blood Coagulation|*; Cardiovascular Diseases|BL/*ET/ME; Diabetic
Angiopathies|BL/*ET/ME; Lipids|*ME
- MeSH Heading
- Adult; Age Factors; Cholesterol|BL; Female; Human; Lipoproteins|ME; Male;
Middle Age; Risk Factors; Sex Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9378
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 57-88-5 (Cholesterol)
Record 55 from database: MEDLINE
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- Title
- Cholesterol autoxidation 1981-1986.
- Author
- Smith LL
- Address
- Department of Human Biological Chemistry and Genetics, University of Texas
Medical Branch, Galveston 77550.
- Source
- Chem Phys Lipids, 1987 Jul-Sep, 44:2-4, 87-125
- Abstract
- Literature published between 1980 and 1986 dealing broadly with the topic of
cholesterol autoxidation is reviewed. The review builds on the detailed 1981
monographic treatment of the topic by the author and covers new items of
chemistry, analysis, and metabolism.
- Language of Publication
- English
- Unique Identifier
- 88027380
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document
- MeSH Heading (Major)
- Cholesterol|*/AN/ME; Sterols|*/AN/ME
- MeSH Heading
- Animal; Food Analysis; Human; Oxidation-Reduction; Support, Non-U.S. Gov't;
Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0009-3084
- Country of Publication
- NETHERLANDS
- CAS Registry/EC Number
- 0 (Sterols); 57-88-5 (Cholesterol)
Record 56 from database: MEDLINE
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- Title
- Cholesterol crystal embolization: a review of 221 cases in the English
literature.
- Author
- Fine MJ; Kapoor W; Falanga V
- Address
- Department of Internal Medicine, University of Pittsburgh, PA.
- Source
- Angiology, 1987 Oct, 38:10, 769-84
- Abstract
- Cholesterol crystal embolization (CCE) frequently presents with nonspecific
manifestations that mimic other systemic diseases. The authors reviewed 221
cases of histologically proven CCE in the English literature to define the
clinical, laboratory, and pathologic characteristics of this disorder. CCE
affected predominantly elderly males (mean age sixty-six) with a frequent
history of hypertension (61%), atherosclerotic cardiovascular disease (44%),
renal failure (34%), and aortic aneurysms (25%) at presentation. At least one
possible predisposing factor was present in 31% and included operative and
radiological vascular procedures and the use of anticoagulants. Cutaneous
findings (34%) and renal failure (50%) were two of the most common clinical
findings throughout the course of CCE. The nonspecific signs and symptoms
included: fever (7%), weight loss (7%), myalgias (4%), and headache (3%).
Premortem diagnoses were established in 31% of patients most commonly by biopsy
of the muscle, skin, and kidney. Mortality was high (81%) and was most commonly
due to multifactorial, cardiac, and renal etiologies. The authors conclude that
CCE should be strongly considered in elderly patients with atherosclerotic
vascular disease who have the onset of renal insufficiency and cutaneous
manifestations. CCE may be confirmed by a skin or muscle biopsy.
- Language of Publication
- English
- Unique Identifier
- 88021943
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document
- MeSH Heading (Major)
- Cholesterol|*; Embolism|*/DI/ME/PA
- MeSH Heading
- Crystallization; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES
- ISSN
- 0003-3197
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 57 from database: MEDLINE
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- Title
- Hypocholesterolemic effects of oat and bean products.
- Author
- Anderson JW; Gustafson NJ
- Address
- Medical Service, Veterans Administration Medical Center, Lexington, KY.
- Source
- Am J Clin Nutr, 1988 Sep, 48:3 Suppl, 749-53
- Abstract
- Oat and bean products, which contain large amounts of water-soluble fiber,
are particularly effective hypocholesterolemic agents. Recent experiments with
human subjects using these products as supplements to the diet are reviewed.
High-carbohydrate, high-fiber diets offer a nutritious, economical, and readily
accepted means to reduce serum cholesterol.
- Language of Publication
- English
- Unique Identifier
- 88324231
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document
- MeSH Heading (Major)
- Cereals|*; Cholesterol|*BL; Dietary Fiber|*PD; Legumes|*
- MeSH Heading
- Adult; Female; Human; Hypercholesterolemia|DH; Male
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW LITERATURE
- ISSN
- 0002-9165
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 58 from database: MEDLINE
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- Title
- Alterations in lipid metabolism induced by antihypertensive therapy.
- Author
- Amery A; Lijnen P
- Address
- Department of Pathophysiology, Catholic University of Leuven, Belgium.
- Source
- Drugs, 1988, 36 Suppl 2:, 1-5
- Abstract
- Adverse effects on serum triglycerides and cholesterol fractions have been
reported in hypertensive patients treated with diuretics and non-selective
beta-blockers. However, the changes induced by cardioselective beta-blockers and
those with intrinsic sympathomimetic activity (ISA) or by alpha-blockers have
been shown to be more favourable. In addition, evidence suggests that calcium
antagonists and angiotensin-converting enzyme (ACE) inhibitors have little
effect on serum lipid concentrations in hypertensive patients, although until
now only diuretics and beta-blockers without ISA have been shown to reduce
morbidity and mortality.
- Language of Publication
- English
- Unique Identifier
- 89106958
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document
- MeSH Heading (Major)
- Antihypertensive Agents|*AE; Cholesterol|*BL; Lipoproteins|*BL;
Triglycerides|*BL
- MeSH Heading
- Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0012-6667
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antihypertensive Agents); 0 (Lipoproteins); 0 (Triglycerides); 57-88-5
(Cholesterol)
Record 59 from database: MEDLINE
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- Title
- Prevalence of diabetic retinopathy and evaluation of risk factors. A review
of 1,005 diabetic clinic patients.
- Author
- Mouton DP; Gill AJ
- Address
- Department of Ophthalmology, University of Stellenbosch and Tygerberg
Hospital, Parowvallei, CP.
- Source
- S Afr Med J, 1988 Oct 15, 74:8, 399-402
- Abstract
- One thousand and five diabetic patients were evaluated ophthalmologically
and classified into one of four groups according to the retinopathy status of
the worst of their eyes. The presence of various factors and their influence on
retinopathy status were evaluated. Race, duration of diabetes, type of
treatment, the presence of hypertension, a high serum cholesterol level, smoking
and the presence of systemic complications of diabetes were found to have a
statistically important influence on retinopathy status. Sex and type of
diabetes had no such influence.
- Language of Publication
- English
- Unique Identifier
- 89044390
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document
- MeSH Heading (Major)
- Diabetic Retinopathy|*ET
- MeSH Heading
- Cholesterol|BL; Diabetes Mellitus|DH; Female; Human; Hypertension|CO; Male;
Racial Stocks; Risk Factors; Sex Factors; Smoking; Time Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE
- ISSN
- 0038-2469
- Country of Publication
- SOUTH AFRICA
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 60 from database: MEDLINE
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- Title
- The biological actions and potential clinical significance of dietary
omega-3 fatty acids.
- Author
- Gorlin R
- Address
- Department of Medicine, Mount Sinai Medical Center, New York City, NY 10029.
- Source
- Arch Intern Med, 1988 Sep, 148:9, 2043-8
- Abstract
- The exploration of the effects of fish oil in cardiovascular disease and
inflammation seems to be a promising avenue of research. There is evidence
indicating the role of marine oils in inhibiting coagulation and platelet,
leukocyte, and T-lymphocyte function. Moderate amounts of fish oil reduce serum
triglyceride and very-low-density lipoprotein levels, while effects on
cholesterol, high-density lipoprotein, and low-density lipoprotein levels are
unpredictable except at extremely large doses. Putative actions in lowering
blood pressure and limiting myocardial infarct size require further study. The
clinician needs to be aware of the dose- and time-dependent nature of the
measurable effects of fish oil. The folly of recommending two to four capsules
per day is contrasted with the ten to 30 capsules required to produce a specific
desired effect.
- Language of Publication
- English
- Unique Identifier
- 88325760
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document
- MeSH Heading (Major)
- Dietary Fats, Unsaturated|*PD; Fatty Acids, Essential|AD/*PH/TU; Fatty
Acids, Unsaturated|*PD; Fish Oils|AD/*ME/TU; Food, Fortified|*
- MeSH Heading
- Animal; Atherosclerosis|PC; Blood Platelets|DE; Cholesterol|BL;
Dose-Response Relationship, Drug; Fishes; Human; Hypertension|PC;
Inflammation|PC; Lipoproteins|BL; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0003-9926
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Dietary Fats, Unsaturated); 0 (Fatty Acids, Essential); 0 (Fatty Acids,
Unsaturated); 0 (Fish Oils); 0 (Lipoproteins); 0 (Triglycerides); 57-88-5
(Cholesterol)
Record 61 from database: MEDLINE
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- Title
- Clinical applications of fish oils [see comments]
- Author
- Yetiv JZ
- Address
- Department of Emergency Medicine, Sequoia Hospital, Redwood City, Calif.
- Source
- JAMA, 1988 Aug 5, 260:5, 665-70
- Abstract
- Fish oil supplements are currently being nationally advertised, and many
physicians are being queried about their clinical utility. Epidemiologic studies
reveal a low incidence of cardiovascular disease in people, such as the Eskimos,
who eat large amounts of seafood. Cardiovascular health may be improved because
fish and fish oil supplements lower plasma lipid levels (especially
triglycerides), inhibit platelet aggregation, and may decrease blood pressure
and viscosity and increase high-density lipoprotein (HDL) levels. Preliminary
observations also suggest a potential future role for fish oils in the treatment
of some autoimmune diseases, such as atopic dermatitis, psoriasis, and
rheumatoid arthritis. Patients with serum triglyceride levels greater than 5.64
mmol/L and/or cholesterol levels greater than 7.75 mmol/L refractory to dietary
management may benefit from a medically supervised trial of fish oil
supplements. Data currently available are insufficient to recommend fish oil
supplements for the general public, or for patients with other diseases, and
side effects must also be considered. These include occasional adverse lipid
changes, potential for bleeding and vitamin E deficiency, and, with some
preparations, vitamin A and D toxicity.
- Language of Publication
- English
- Unique Identifier
- 88275107
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document
- MeSH Heading (Major)
- Fish Oils|AE/*TU
- MeSH Heading
- Adolescence; Animal; Anti-Inflammatory Agents|ANTIINFLAMMATORY AGENTS;
Blood|DE; Blood Pressure|DE; Child; Cholesterol|BL; Fatty Acids|ME; Female;
Human; Immunity|DE; Neoplasms|PC; Pregnancy
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0098-7484
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Fatty Acids); 0 (Fish Oils); 57-88-5 (Cholesterol)
Record 62 from database: MEDLINE
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- Title
- Cholesterol embolism causing bleeding gastric ulcers.
- Author
- Forouhar FA; Mohit M; Gardner P; Smith N
- Address
- Pathology Department, University of Connecticut Health Center, Farmington
06032.
- Source
- Ann Clin Lab Sci, 1988 May-Jun, 18:3, 260-5
- Abstract
- Two cases of atheromatous embolism of the small arteries of the stomach are
reported. Insofar as has been ascertained, they are the first reported cases in
the literature which presented symptoms of severe gastric bleeding and were
found to have bleeding gastric ulcers on endoscopy. Both patients were
successfully treated surgically, and their ulcers were found to be secondary to
small arteriolar occlusions owing the atherosclerotic embolization. Awareness of
clinicians as well as pathologists of this phenomenon in elderly males with
symptoms of abdominal pain and other upper gastrointestinal symptoms unrelated
to the ingestion of food is stressed. Pathophysiology of atherosclerotic emboli
is also discussed.
- Language of Publication
- English
- Unique Identifier
- 88267907
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document
- MeSH Heading (Major)
- Cholesterol|*ME; Embolism|*CO/ME; Peptic Ulcer Hemorrhage|*ET
- MeSH Heading
- Aged; Case Report; Female; Human; Male; Stomach Ulcer|ET
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES
- ISSN
- 0091-7370
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 63 from database: MEDLINE
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- Title
- Genetic control of susceptibility to atherosclerosis (with special emphasis
on the role of the macrophage).
- Author
- Clarke A; Stewart-Phillips JL; Skamene E
- Address
- Department of Medicine, Montreal General Hospital, Quebec, Canada.
- Source
- Clin Invest Med, 1987 Nov, 10:6, 499-512
- Abstract
- The pathogenesis of atherosclerosis involves a complex interplay of arterial
endothelium, multiple cellular constituents, and circulating
lipo/apolipoproteins. Early work implicated a single etiology--either excess of
circulating lipids, disruption of endothelial integrity, or clonal proliferation
of smooth muscle cells. However, current research supports a hypothesis unifying
endothelial disruption with lipid imbibation. The macrophage is recognized as
having an integral role in atherogenesis due to its capacity to adhere to
endothelium, internalize and metabolize lipids, and liberate proteases,
apolipoproteins, and mitogens. Genetically determined susceptibility or
resistance to atherosclerosis has long been described in animals and man, and
differences in lipo/apolipoproteins have been proposed to explain these
variations. Genetically defined variants of inbred mice have been used to pursue
hereditary influences in atherogenesis. Strain variations in lipid metabolism
have been advanced as one possibility to explain a polygenic mode of
inheritance--those strains most replete in cholesterol-enriched lipoproteins
demonstrating the greatest susceptibility. However, there is now a substantial
body of evidence suggesting that the diverse functions of the macrophage may be
the mechanism underlying the genetic polymorphism in atherosclerosis.
Recombinant inbred strains of mice may serve as a vehicle through which this
concept can be explored.
- Language of Publication
- English
- Unique Identifier
- 88151285
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document
- MeSH Heading (Major)
- Arteriosclerosis|*GE; Atherosclerosis|ET/*GE; Macrophages|ME/*PH/SE
- MeSH Heading
- Animal; Cholesterol|GE; Coronary Arteriosclerosis|GE; Disease
Susceptibility; Endothelium, Vascular|IN; Human; Lipoproteins|BL/ME; Mice
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0147-958X
- Country of Publication
- CANADA
- CAS Registry/EC Number
- 0 (Lipoproteins); 57-88-5 (Cholesterol)
Record 64 from database: MEDLINE
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- Title
- Dietary copper: a powerful determinant of cholesterolemia.
- Author
- Klevay LM
- Address
- United States Department of Agriculture, Human Nutrition Research Center,
Grand Forks, North Dakota 58202.
- Source
- Med Hypotheses, 1987 Oct, 24:2, 111-9
- Abstract
- A new hypothesis suggests that deficiency of copper is important in the
etiology and pathophysiology of ischemic heart disease. Several chemicals,
called cholesterotropic and cuprotropic, that affect cholesterolemia also affect
copper metabolism. Responses to some of these chemicals that have been tested in
humans were compared on a molar basis. Dietary copper was approximately one
hundred times as active in lowering cholesterol in plasma than was clofibrate
which, in turn was six times as active as dietary fat. Dietary copper may be a
powerful determinent of cholesterolemia.
- Language of Publication
- English
- Unique Identifier
- 88065179
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Copper|*DF/PD; Hypercholesterolemia|DT/*ET
- MeSH Heading
- Animal; Anticholesteremic Agents|TU; Coronary Disease|BL; Human; Risk
Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0306-9877
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Anticholesteremic Agents); 57-88-5 (Cholesterol); 7440-50-8 (Copper)
Record 65 from database: MEDLINE
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- Title
- Exercise and obesity.
- Author
- Pacy PJ; Webster J; Garrow JS
- Address
-
- Source
- Sports Med, 1986 Mar-Apr, 3:2, 89-113
- Abstract
- Obesity, prevalent in industrialised societies, is most usefully categorised
by means of the body mass index (BMI-weight/height2). A body mass index of
greater than 25 is associated with increasingly poor prognosis. Weight reduction
has been shown to be beneficial with respect to both mortality and morbidity.
Excess weight results from an imbalance between energy input and expenditure in
favour of the former. Weight reduction may be promoted by reducing energy input
and/or stimulating expenditure. It is tempting to postulate that inactivity may
be a factor in both the development and subsequent continuation of obesity via
an effect on energy intake, fat-free mass or energy expenditure. Although
available data are by no means conclusive, the majority of evidence suggests
that obesity is not associated with either reduced activity or energy
expenditure. Likewise, exercise appears not to promote a change in body
composition in favour of lean body mass or have a prolonged thermogenic effect
beyond the duration of the activity. Exercise alone appears largely ineffective
regarding weight loss and almost certainly has to be coupled with calorie
reduction. It must be remembered that the exercise tolerance in the severely
obese (BMI greater than 40) is very poor. Such individuals must be closely
supervised during a specifically graded programme. What is also apparent is the
high drop-out rate of individuals recruited into exercise programmes. In those
who voluntarily engage in physical activity, the incidence of ischaemic heart
disease may be reduced, which may or may not be related to a direct exercise
effect on known cardiovascular risk factors. Cigarette smoking is usually less
common and general life-style may be more prudent. Whether exercise in obese
subjects could have a similar effect remains unknown. Although much of the data
on exercise in general and on obesity in particular are negative, it appears
unwise to adopt a totally nihilistic approach. Increased physical activity
should be encouraged as it is possible that the discipline involved in regularly
undertaking such activity may be more conducive to weight loss, a feeling of
well-being and fitness and a general change of life-style for the better. Long
term it may also afford additional benefit by reducing liability to ischaemic
heart disease.
- Language of Publication
- English
- Unique Identifier
- 86179154
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document
- MeSH Heading (Major)
- Exertion|*; Obesity|CO/MO/*TH
- MeSH Heading
- Animal; Basal Metabolism; Body Composition; Body Weight; Cardiovascular
Diseases|CO; Cholesterol|BL; Data Collection|MT; Energy Intake; Energy
Metabolism; Exercise Therapy; Female; Human; Insulin|BL; Life Style;
Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Male;
Muscles|ME; Physical Fitness; Proteins|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0112-1642
- Country of Publication
- NEW ZEALAND
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL Cholesterol);
11061-68-0 (Insulin); 57-88-5 (Cholesterol)
Record 66 from database: MEDLINE
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- Title
- Nutritional contributors to cardiovascular disease in the elderly.
- Author
- Kannel WB
- Address
-
- Source
- J Am Geriatr Soc, 1986 Jan, 34:1, 27-36
- Abstract
- Cardiovascular disease, so common in the elderly, has become an urgent
public health concern. Major contributing factors include hypertension,
dyslipidemia, impaired glucose tolerance, physical indolence, and cigarette
smoking. Diet plays a major role in atherogenesis by its influence in blood
lipids, blood pressure, and glucose tolerance, although its impact in the
elderly is speculative owing to a paucity of direct evidence. But a rationale
exists. Most cardiovascular risk factors are more prevalent in the elderly than
in the young adult. The rise in blood pressure and blood lipids with advancing
age is not inevitable. Diet may contribute to hypertension through an excess of
calories, saturated fat, cholesterol, or salt and a deficiency of potassium,
calcium, and magnesium. Antiatherogenic diets low in saturated fat and
cholesterol, rich in fiber, and with substitution of polyunsaturated fat and
restricted calories tend to normalize serum lipids and to cause lesions to
involute. Emphasis on vegetable protein and fiber-rich food has merit because
they provide more fiber, polyunsaturated fatty acids, magnesium, selenium,
complex carbohydrate, potassium, and copper, and less cholesterol, saturated
fat, and sodium. The recommended fat-modified diets are adequate in protein,
vitamins, and minerals and need not be deficient in any nutrient or economically
nonfeasible. The accelerating decline in cardiovascular mortality, which has
included the elderly, indicates that such disease is controllable and not
inevitable, even in the elderly. The decrease has occurred concurrently with
reduced consumption of saturated fat and cholesterol, increased use of vegetable
oils, and improved levels of cardiovascular risk factors.
- Language of Publication
- English
- Unique Identifier
- 86086900
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- MeSH Heading (Major)
- Aging|*; Cardiovascular Diseases|*ET/MO; Dietary Fats|*AE; Nutrition|*
- MeSH Heading
- Adolescence; Adult; Age Factors; Aged; Alcohol Drinking; Blood Pressure;
Cholesterol|BL; Energy Intake; Female; Follow-Up Studies; Human;
Hypertension|ET; Male; Middle Age; Risk; Sex Factors; Smoking; United States
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-8614
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Dietary Fats); 57-88-5 (Cholesterol)
Record 67 from database: MEDLINE
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- Title
- The effect of drugs on bile flow and composition. An overview.
- Author
- Okolicsanyi L; Lirussi F; Strazzabosco M; Jemmolo RM; Orlando R; Nassuato G;
Muraca M; Crepaldi G
- Address
-
- Source
- Drugs, 1986 May, 31:5, 430-48
- Abstract
- Many drugs are eliminated via the hepatobiliary route, after
biotransformation in the liver. Some of them may affect bile flow and/or the
hepatic secretion of biliary lipids such as bile acids, cholesterol and
phospholipids. Bile acids are the most potent agents which increase bile flow,
especially unconjugated bile acids. Other drugs which increase bile flow include
phenobarbitone (phenobarbital), theophylline, glucagon and insulin. In contrast,
ethacrynic acid, amiloride, ouabain, oestrogens and chlorpromazine are among
those agents which decrease bile flow. Biliary bile acid secretion is altered by
a variety of drugs, including cheno- and ursodeoxycholic acids (CDCA and UCDA),
the bile acid sequestrants cholestyramine and colestipol, and ethinyloestradiol.
The composition of bile can also be altered by drug therapy. Thus, clofibrate
increases biliary cholesterol secretion, and reduces bile acid concentrations,
without altering biliary phospholipid concentrations. However, other clofibrate
derivatives may produce changes of a different pattern, suggesting that the risk
of developing gallstones may differ for each derivative. Nicotinic acid and
d-thyroxine also increase biliary cholesterol saturation, while CDCA and UDCA
reduce biliary cholesterol concentration. The potential consequences of
drug-induced changes in bile flow and composition extend to the liver, the
gallbladder and the intestine. If adverse effects are to be avoided, further
study in this often overlooked area is required.
- Language of Publication
- English
- Unique Identifier
- 86219857
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document
- MeSH Heading (Major)
- Bile|*SE; Cholagogues and Choleretics|*; Liver|ME/*SE
- MeSH Heading
- Animal; Bile Acids and Salts|SE; Cats; Chlorpromazine|PD; Cholesterol|SE;
Clofibrate|PD; Colchicine|PD; Comparative Study; Dehydrocholic Acid|PD;
Diuretics|PD; Dogs; Enterohepatic Circulation|DE; Estrogens|PD; Glucagon|PD;
Guinea Pigs; Hamsters; Human; Insulin|PD; Macaca mulatta; Phospholipids|ME/SE;
Rabbits; Rats; Rifampin|PD; Rifamycins|PD; Somatostatin|PD; Support, Non-U.S.
Gov't; Theophylline|PD; Ursodeoxycholic Acid|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0012-6667
- Country of Publication
- AUSTRALIA
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 0 (Cholagogues and Choleretics); 0 (Diuretics); 0
(Estrogens); 0 (Phospholipids); 0 (Rifamycins); 11061-68-0 (Insulin); 128-13-2
(Ursodeoxycholic Acid); 13292-46-1 (Rifampin); 50-53-3 (Chlorpromazine);
51110-01-1 (Somatostatin); 57-88-5 (Cholesterol); 58-55-9 (Theophylline);
637-07-0 (Clofibrate); 64-86-8 (Colchicine); 81-23-2 (Dehydrocholic Acid);
9007-92-5 (Glucagon)
Record 68 from database: MEDLINE
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- Title
- Hepatocytic lipoprotein receptors and intracellular lipoprotein catabolism.
- Author
- Havel RJ; Hamilton RL
- Address
- Cardiovascular Research Institute, University of California, San Francisco
94143-0130.
- Source
- Hepatology, 1988 Nov-Dec, 8:6, 1689-704
- Abstract
- Hepatocytes, as the major site of synthesis and terminal catabolism of
plasma lipoproteins, exert the major regulatory influence on the concentration
of atherogenic lipoproteins in blood plasma and may thereby influence the rate
of atherogenesis. The LDL receptor on the microvillous sinusoidal surface of
hepatocytes mediates the catabolism of remnants of triglyceride-rich
lipoproteins and LDL. Binding of VLDL remnants to the receptor, mediated by apo
E, is of very high affinity and presumably multivalent, whereas binding of LDL,
mediated by apo B-100, is monovalent and of lower affinity, accounting for the
much longer residence time of the latter in the blood. The magnitude of the
influx of lipoprotein particles into hepatocytic endosomal compartments dwarfs
that of other macromolecules undergoing receptor-mediated endocytosis and
terminal catabolism in lysosomes of these cells. The intracellular compartments
and processing steps in hepatocytic lipoprotein uptake and degradation are
essentially the same as those described for other ligands in the liver and other
cells. Receptors with bound lipoproteins migrate into coated pits which become
coated vesicles. These vesicles uncoat and fuse to form CURL vesicles and
tubules near the cell surface where most receptors are recycled, presumably via
receptor-rich appendages that become separated from the vesicles. CURL vesicles
become mature MVBs as they migrate to the Golgi/bile canalicular pole of
hepatocytes, where they fuse with putative Golgi-derived primary lysosomes and
are transformed into heterophagic secondary lysosomes. MVBs also contain a
receptor-rich appendage that may recycle some receptors directly to the cell
surface or through adjacent Golgi compartments. Dilated ends of trans-Golgi
cisternae contain nascent VLDL undergoing packaging for secretion following
their synthesis and assembly in the endoplasmic reticulum. Because these
"forming secretory vesicles" resemble remnant-filled MVBs, occur in a
similar location in the Golgi area of hepatocytes and coisolate in centrifugal
fractions of liver homogenates, there has been considerable confusion about the
identity of these compartments. With the aid of specific endocytic and exocytic
markers, highly purified and morphologically intact endosomal and Golgi
compartments can now be obtained from rat liver homogenates. The availability of
these and similar fractions of defined purity should facilitate investigation of
the hepatocytic processing of endocytosed and secreted macromolecules. Although
chylomicron remnants are also taken up by receptor-mediated endocytosis, the
nature of the hepatocytic remnant receptor remains elusive.(ABSTRACT TRUNCATED
AT 400 WORDS)
- Language of Publication
- English
- Unique Identifier
- 89053252
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document
- MeSH Heading (Major)
- Lipoproteins|*ME; Liver|CY/*ME/UL; Receptors, Cell Surface|*ME
- MeSH Heading
- Animal; Cholesterol|ME; Chylomicrons|ME; Endocytosis; Human; Lipoproteins,
HDL|ME; Lipoproteins, LDL|ME; Lysosomes|ME; Rabbits; Rats
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0270-9139
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Chylomicrons); 0 (Lipoproteins); 0 (Lipoproteins, HDL); 0 (Receptors,
Cell Surface); 0 (Receptors, Lipoprotein); 57-88-5 (Cholesterol)
Record 69 from database: MEDLINE
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- Title
- Dietary fibre and lipid metabolism.
- Author
- Kritchevsky D
- Address
-
- Source
- Int J Obes, 1987, 11 Suppl 1:, 33-43
- Abstract
- The influence of dietary fibre on lipid metabolism can be assessed at
several levels. In animal studies it is possible to investigate the effects of
fibre on serum and tissue lipid levels, on lipid absorption and excretion and,
in specific instances, on experimental atherosclerosis. In man we are limited to
examination of blood lipid and lipoprotein levels and on patterns of lipid
excretion. Ershoff and his co-workers (eg) were among the first to demonstrate
beneficial effects of fibre on serum and liver cholesterol levels in
cholesterol-fed rats. They also showed that not all that we call fibre is
hypocholesterolaemic. Cellulose, for instance, caused increases in liver
cholesterol levels in rats. Cellulose also leads to increased levels of carcass
cholesterol. Experiments in chickens, rabbits and monkeys have shown cellulose
to exert the least beneficial effect on atherosclerosis or aortic sudanophilia.
In man the insoluble fibres such as bran or cellulose are not
hypocholesterolaemic, whereas soluble fibres such as guar gum or pectin are. The
effects are also reflected in levels of high and low density lipoproteins.
Studies relating to mechanism(s) of fibre action have shown that fibre may
increase cholesterol and bile acid excretion and, in some cases, may affect
faecal bile acid composition. Fibres have been shown to bind bile acids in
vitro, the extent of binding being a function of both the type of fibre used and
the type of bile acid or bile salt being studied. Fibre has also been shown to
bind other lipids. Fibre also influences the rate of cholesterol absorption. To
date most results can be classified according to the type of fibre used, ie
soluble or insoluble; ionic or non-ionic. Our added understanding of modes of
action of fibre will depend on better ability to relate structure to function.
- Language of Publication
- English
- Unique Identifier
- 87193511
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document
- MeSH Heading (Major)
- Dietary Fiber|*PD; Lipids|BL/*ME
- MeSH Heading
- Animal; Atherosclerosis|BL/DH; Bile Acids and Salts|ME; Cholesterol|BL;
Human; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0307-0565
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 57-88-5 (Cholesterol)
Record 70 from database: MEDLINE
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- Title
- Receptor interactions controlling lipoprotein metabolism.
- Author
- Weisgraber KH; Innerarity TL; Rall SC Jr; Mahley RW
- Address
-
- Source
- Can J Biochem Cell Biol, 1985 Aug, 63:8, 898-905
- Abstract
- Lipoprotein receptors play a central role in lipoprotein metabolism and a
major role in cholesterol homeostasis. The most completely characterized
lipoprotein receptor is the LDL (low density lipoprotein) or apo-B,E(LDL)
receptor. The apo-B,E(LDL) receptor is present on both hepatic and extrahepatic
cells and is responsible for the metabolism of a major portion of plasma LDL.
Binding and internalization of LDL particles by this receptor initiates a series
of intracellular events, resulting in the regulation of cellular cholesterol
metabolism. In addition to the apo-B on LDL interacting with the apo-B,E(LDL)
receptor, the apo-E on apo-E-containing lipoproteins is also capable of
interacting and regulating intracellular cholesterol metabolism. The liver has
also been shown to contain a second distinct lipoprotein receptor that is
specific for apo-E. This receptor has been demonstrated on hepatic membranes
from humans, dogs, and swine and is referred to as the apo-E receptor. This
receptor may be responsible for the clearance of chylomicron remnants from
plasma by the liver and may participate in reverse cholesterol transport. Thus,
apo-E is a major determinant in lipoprotein metabolism and cholesterol
homeostasis. The receptor binding properties of apo-E are well characterized,
and a series of structural variants, several with lipoprotein binding defects,
have been identified. Studies of the binding activity of these
receptor-defective apo-E variants have helped to define the receptor binding
domain of apo-E.(ABSTRACT TRUNCATED AT 250 WORDS)
- Language of Publication
- English
- Unique Identifier
- 86052867
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- MeSH Heading (Major)
- Lipoproteins|*ME; Receptors, Cell Surface|*ME
- MeSH Heading
- Amino Acid Sequence; Animal; Apolipoproteins E|ME; Binding Sites;
Cholesterol|ME; Homeostasis; Human; Models, Biological; Protein Binding;
Structure-Activity Relationship
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0714-7511
- Country of Publication
- CANADA
- CAS Registry/EC Number
- 0 (Apolipoproteins E); 0 (Lipoproteins); 0 (Receptors, Cell Surface); 0
(Receptors, Lipoprotein); 57-88-5 (Cholesterol)
Record 71 from database: MEDLINE
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- Title
- A histochemical investigation on the percutaneous absorption of vitamin D
synthesized into the mammal epidermis.
- Author
- Silveira SR; Hadler WA
- Address
-
- Source
- Acta Histochem, 1985, 77:1, 11-8
- Abstract
- The vitamin D transepidermis absorption was studied by means of a
histochemical technique suitable to detect this vitamin and to discriminate it
from cholesterol and its esters. Such technique shows vitamin D inside the mast
cell granules. As the mast cell granules contain metachromatic substances its
own histochemical reactivity must be previously blocked by methylation. After
this treatment the mast cell granules do not stain by toluidine blue and do not
react to the peracetic acid-toluidine blue reaction. However, the granules
remains reactive to alkaline permanganate-toluidine blue and to alkaline
permanganate-Schiff reactions. These results show that the mast cell granules do
not contain cholesterol but they contain vitamin D. The lack of cholesterol
suggests that vitamin D is not synthesized inside the granules. As the mast
cells may appears within the epidermis or in close relationship with the
epidermis, although it is placed into the superficial dermis, it was admitted
that the mast cells uptake vitamin D contained inside the epidermis
intercellular compartment. In such instances, the vitamin D synthesized by the
keratinocytes enter the intercellular compartment, where its synthesis
accomplishes, and migrate towards the basement membrane. At the basal epidermis
layer or after passing through the basement membrane the vitamin D is taken up
by mast cells, where it is stored inside its granules.
- Language of Publication
- English
- Unique Identifier
- 86046847
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document
- MeSH Heading (Major)
- Cholecalciferol|*ME; Skin|*ME
- MeSH Heading
- Absorption; Animal; Basement Membrane|ME; Cats; Cholesterol|ME; Cytoplasmic
Granules|ME; Dogs; Histocytochemistry; Human; Mast Cells|ME; Mice; Rabbits; Rats
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0065-1281
- Country of Publication
- GERMANY, EAST
- CAS Registry/EC Number
- 57-88-5 (Cholesterol); 67-97-0 (Cholecalciferol)
Record 72 from database: MEDLINE
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- Title
- Physiological and metabolic effects of dietary fiber.
- Author
- Anderson JW
- Address
-
- Source
- Fed Proc, 1985 Nov, 44:14, 2902-6
- Abstract
- William Beaumont noted the gastric effects of vegetable fiber and suggested
that dietary fiber may provide health benefits. In the last decade investigators
documented the physiological effects of fiber on gastric emptying, intestinal
nutrient absorption rates, and colon function. Further clinical investigation
and much more of the type of repetitive observations pioneered by Beaumont are
required to definitively establish the physiological effects of fiber on
gastrointestinal physiology. High-fiber intake provides well-established
benefits for persons with diabetes: it lowers insulin requirements, provides
better control of blood glucose, and reduces serum lipids. Foods rich in soluble
fiber, such as oat or bean products, lower cholesterol significantly for persons
with hypercholesterolemia and for healthy young subjects. High-fiber foods also
lower serum triglycerides and blood pressure. Several studies indicate that high
intake of fiber protects against coronary heart disease.
- Language of Publication
- English
- Unique Identifier
- 86030718
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document
- MeSH Heading (Major)
- Colon|MI/*PH; Dietary Fiber|AD/*PD/TU; Intestine, Small|*PH; Stomach|*PH
- MeSH Heading
- Bacteria|ME; Bile Acids and Salts|ME; Cereals; Cholesterol|BL; Diabetes
Mellitus, Insulin-Dependent|DH; Diabetes Mellitus, Non-Insulin-Dependent|DH;
Fatty Acids, Volatile|ME; Feces; Gastric Emptying; Gastrointestinal Motility;
Glucose|ME; Human; Hypercholesterolemia|DH; Insulin|BL; Intestinal Absorption;
Lipoproteins, LDL Cholesterol|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0014-9446
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 0 (Fatty Acids, Volatile); 0 (Lipoproteins, LDL
Cholesterol); 11061-68-0 (Insulin); 50-99-7 (Glucose); 57-88-5 (Cholesterol)
Record 73 from database: MEDLINE
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- Title
- Dietary protein effects on cholesterol and lipoprotein concentrations: a
review.
- Author
- Forsythe WA; Green MS; Anderson JJ
- Address
-
- Source
- J Am Coll Nutr, 1986, 5:6, 533-49
- Abstract
- Different dietary proteins exert different effects on plasma cholesterol
concentrations. Animal studies have shown that animal proteins, most notably
casein, increase plasma total cholesterol concentrations compared with vegetable
proteins, such as soy. Soy protein has been shown to be hypocholesterolemic in
rats, swine, primates, and rabbits. Epidemiologic studies have disclosed that
vegetarians have lower mean plasma cholesterol concentrations than populations
consuming diets of mixed proteins, but it is unclear whether this effect results
specifically from the animal or vegetable nature of the protein. In human
clinical experiments, substituting soy protein for mixed protein reduces plasma
total cholesterol concentration in hypercholesterolemic subjects, but it causes
only a small, nonsignificant change in persons with normal plasma cholesterol
concentrations. The mechanism responsible for the effects of different proteins
on plasma cholesterol concentrations has not been established. One hypothesis
suggests that animal proteins, which have a greater content of phosphorylated
amino acids than vegetable proteins, interfere with bile acid reabsorption.
Another hypothesis suggests that the amino acid content of the protein affects
cholesterol absorption, tissue storage, synthesis, and excretion. The dietary
protein may also alter cholesterol metabolism by affecting plasma hormone
concentrations, either postprandially or over weeks to months. Among the
hormones thought to be affected by dietary protein source are insulin, glucagon,
and thyroid hormones. Gastrointestinal hormones, such as gastrointestinal
inhibitory polypeptide, may also be affected by dietary protein.
- Language of Publication
- English
- Unique Identifier
- 87058559
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Dietary Proteins|*PD; Lipoproteins|*BL
- MeSH Heading
- Amino Acids|AN; Animal; Apolipoproteins|BL; Arginine|ME; Digestion;
Glucagon|BL; Human; Insulin|BL; Intestinal Absorption; Lipoproteins, HDL
Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL; Lysine|ME; Saponins|ME;
Sterols|ME; Tissue Distribution
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0731-5724
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Amino Acids); 0 (Apolipoproteins); 0 (Dietary Proteins); 0
(Lipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL
Cholesterol); 0 (Saponins); 0 (Sterols); 11061-68-0 (Insulin); 56-87-1 (Lysine);
57-88-5 (Cholesterol); 7004-12-8 (Arginine); 9007-92-5 (Glucagon)
Record 74 from database: MEDLINE
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- Title
- Lipid markers for atherosclerosis.
- Author
- Kottke BA
- Address
-
- Source
- Am J Cardiol, 1986 Feb 12, 57:5, 11C-17C
- Abstract
- Atherogenesis results from the simultaneous occurrence of 2 important
processes: platelet-endothelial interaction, with its consequences mediated by
the platelet-derived growth factor, and lipid accumulation. Lipid accumulation
results from the balance or imbalance of cellular uptake of lipoproteins versus
the removal of cholesterol esters. Uptake results from activity of the
low-density lipoprotein (LDL) receptor of smooth muscle cells and fibroblasts,
modified LDL receptor and remnant receptors of macrophages. Cholesterol-ester
removal is regulated by apolipoprotein A-l. Low levels of apolipoprotein A-l are
found in most patients with clinically significant coronary artery disease,
suggesting that defects in cellular cholesterol ester removal may play an
important role in atherogenesis.
- Language of Publication
- English
- Unique Identifier
- 86127054
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document
- MeSH Heading (Major)
- Arteriosclerosis|*ET; Atherosclerosis|*ET/ME; Lipids|*ME
- MeSH Heading
- Apolipoproteins A|AN/GE/ME; Binding Sites; Cholesterol|ME; Endothelium|ME;
Human; Lipoproteins|ME; Macrophages|PH; Receptors, LDL|AN
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoprotein A-I); 0 (Apolipoproteins A); 0 (Lipoproteins); 0
(Receptors, LDL); 0 (VLDL receptor); 57-88-5 (Cholesterol)
Record 75 from database: MEDLINE
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- Title
- The future of pharmacological therapy for risk factor reduction.
Hyperlipidaemia.
- Author
- Olsson AG; Mölgaard J
- Address
- Department of Internal Medicine, University Hospital, Linköping, Sweden.
- Source
- Drugs, 1988, 36 Suppl 3:, 115-20
- Abstract
- The European Atherosclerosis Society has produced guidelines for the drug
treatment of hyperlipidaemia. This, of necessity, is lifelong and therefore
should be prescribed only after exclusion of secondary causes for the disorder,
after dietary advice has failed to produce desirable plasma lipid levels and
after careful consideration of the individual case. A plasma lipid-lowering drug
should be efficacious on a long term basis on plasma lipid levels, should fulfil
conditions for long term compliance regarding simplicity of administration and
lack of subjective side effects, have a documented effect on the clinical
endpoint (e.g. myocardial infarction) and be safe on a long term basis. Based on
these conditions, plasma lipid-lowering drugs can be classed as first- or
second-line treatments. At present, examples of first-line drugs are
cholestyramine, nicotinic acid and gemfibrozil, while second-line drugs are
lovastatin, simvastatin, probucol and 'third generation' fibrates. With
increasing experience with the newer drugs regarding clinical efficacy and long
term safety, one hopes that lovastatin, simvastatin and probucol will fulfil all
criteria and become first-line drugs. These have advantages over cholestyramine
and nicotinic acid in terms of better patient compliance.
- Language of Publication
- English
- Unique Identifier
- 89338069
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document
- MeSH Heading (Major)
- Hyperlipidemia|CO/*DT
- MeSH Heading
- Antilipemic Agents|TU; Cholesterol|BL; Human; Risk Factors; Support,
Non-U.S. Gov't; Time Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0012-6667
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antilipemic Agents); 57-88-5 (Cholesterol)
Record 76 from database: MEDLINE
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- Title
- High-performance liquid chromatography of steroid hormones.
- Author
- Makin HL; Heftmann E
- Address
-
- Source
- Monogr Endocrinol, 1988, 30:, 183-234
- Abstract
- Although a considerable amount of work has been carried out in the last ten
years in developing methods for the separation of steroids by HPLC, it is still
not widespread for the reasons discussed above. There is however no doubt that
further developments in HPLC technology, in increasing sensitivity and/or
specificity of detection systems, perhaps with microbore columns, may lead to an
increase in the use of this powerful analytical procedure as an additional
separation method to improve specificity of assay. Solution of the problem of
simple interfacing of HPLC systems with mass spectrometers (discussed in another
chapter by Games) should further increase the application of HPLC. HPLC is of
particular value in providing a means of separating unstable compounds prior to
assay by relatively nonspecific quantitation methods. Most steroids do not fall
into this category, but the steroid vitamin D and its metabolites do and HPLC
has proved in this area to be invaluable (see chapter by Jones & DeLuca).
There are a multiplicity of different HPLC systems for the separation of
steroids, varying in column type (and manufacturer), solvent composition and
method of elution, temperature of elution, etc., and only a few attempts have
been made to rationalise these data. It would therefore seem that a fruitful
area of future study would be the investigation of computerised systems for the
selection and optimisation of HPLC systems for particular steroid separations.
- Language of Publication
- English
- Unique Identifier
- 89159181
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document
- MeSH Heading (Major)
- Chromatography, High Pressure Liquid|*MT; Steroids|*AN/ME
- MeSH Heading
- Adrenal Cortex Hormones|AN/BI; Androgens|AN/BI; Chemistry;
Cholesterol|AN/ME; Estrogens|AN/BI; Human; Progesterone|AN/BI; Receptors,
Steroid|AN
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0077-1015
- Country of Publication
- GERMANY, WEST
- CAS Registry/EC Number
- 0 (Adrenal Cortex Hormones); 0 (Androgens); 0 (Estrogens); 0 (Receptors,
Steroid); 0 (Steroids); 57-83-0 (Progesterone); 57-88-5 (Cholesterol)
Record 77 from database: MEDLINE
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- Title
- The relevance of intrinsic sympathomimetic activity for beta-blocker-induced
changes in plasma lipids.
- Author
- van Brummelen P
- Address
-
- Source
- J Cardiovasc Pharmacol, 1983, 5 Suppl 1:, S51-5
- Abstract
- The possible relevance of intrinsic sympathomimetic activity (ISA) for
beta-blocker-induced changes in plasma lipids was investigated by reviewing the
literature and analyzing the results separately for nonselective beta-blockers,
beta 1-selective beta-blockers, and those possessing ISA. It was confirmed that
with the exception of the nonselective beta-blocker sotalol, beta-blocker
therapy has little influence on the plasma concentrations of total cholesterol
and low-density lipoprotein (LDL)-cholesterol. The small differences in mean
changes in LDL-cholesterol observed among the three groups of beta-blockers are
probably of negligible practical importance. More important differences emerged
from the pooling of data on plasma triglycerides and high-density lipoprotein
(HDL)-cholesterol. Here, beta-blockers possessing ISA showed the smallest mean
increase in triglycerides and an increase in HDL-cholesterol, which compared
favorably with the decrease found for nonselective and beta 1-selective
beta-blockers. Of the individual beta-blockers, pindolol exhibited the most
favorable lipid profile. A close inverse correlation was found between the
changes in triglycerides and HDL-cholesterol in the various studies. This
finding, together with other arguments, supports the view that these changes are
the result of inhibition of lipoprotein lipase by adrenergic mechanisms.
- Language of Publication
- English
- Unique Identifier
- 83190656
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document
- MeSH Heading (Major)
- Adrenergic beta-Antagonists|*PD; Lipids|*BL; Sympathomimetics|*PD
- MeSH Heading
- Cholesterol|BL; Human; Lipoproteins, HDL|BL; Lipoproteins, LDL|BL; Risk;
Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0160-2446
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Adrenergic beta-Antagonists); 0 (Lipoproteins, HDL Cholesterol); 0
(Lipoproteins, HDL); 0 (Lipoproteins, LDL Cholesterol); 0 (Sympathomimetics); 0
(Triglycerides); 57-88-5 (Cholesterol)
Record 78 from database: MEDLINE
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- Title
- The emerging problem of plasma lipid changes during antihypertensive
therapy.
- Author
- Johnson BF
- Address
-
- Source
- J Cardiovasc Pharmacol, 1982, 4 Suppl 2:, S213-21
- Abstract
- After hypertension and smoking, abnormalities of plasma lipids are major
coronary risk factors. Increases in low density lipoprotein (LDL) cholesterol,
or decreases in high density lipoprotein (HLD) cholesterol or the ratio HDL/LDL
are associated with increased risk. Whereas LDL delivers cholesterol to arterial
wall cells. HDL aids clearance and/or inhibits uptake of LDL cholesterol. Some
agents used to reduce risks of high blood pressure can also disturb lipoprotein
levels and may increase associated coronary risk levels. Thiazides increase
triglycerides (TG) and increase total cholesterol. However, the HDL/LDL ratio
shows no important change in our recent studies.TG elevation may result from
increased synthesis secondary to increased plasma levels of glucose and insulin.
In several studies, propranolol also caused elevation of TG. This has been the
most consistent finding in the few studies of other beta blockers, including
metoprolol, atenolol, and pindolol. These studies have generally shown no change
in total cholesterol, but some showed reduction in HDL cholesterol in patients
on propranolol.
- Language of Publication
- English
- Unique Identifier
- 82218278
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document
- MeSH Heading (Major)
- Antihypertensive Agents|*AE; Hypertension|*BL/DT; Lipids|*BL
- MeSH Heading
- Adrenergic beta-Antagonists|AE; Cholesterol|BL; Coronary Disease|ET;
Diuretics|AE; Drug Therapy, Combination; Human; Hyperlipidemia|CI; Lipoproteins,
HDL|BL; Lipoproteins, LDL|BL; Risk; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0160-2446
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Adrenergic beta-Antagonists); 0 (Antihypertensive Agents); 0 (Diuretics);
0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL); 0 (Lipoproteins, LDL
Cholesterol); 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 79 from database: MEDLINE
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- Title
- Coronary atherosclerosis and plasma lipoproteins: epidemiology and
pathophysiologic considerations.
- Author
- Miller NE
- Address
-
- Source
- J Cardiovasc Pharmacol, 1982, 4 Suppl 2:, S190-5
- Abstract
- A variety of epidemiologic, biochemical, and experimental studies have
established a direct relationship between low density lipoprotein (LDL)
cholesterol concentration and the risk of developing ischemic heart disease. An
even stronger inverse relationship has been demonstrated between high density
lipoprotein (HDL) cholesterol and the risk of ischemic heart disease (IHD). Both
of these associations reflect underlying relationships to atherogenesis. The
mechanism by which elevated LDL levels lead to cholesterol ester deposition in
arterial smooth muscle cells and/or macrophages is not clear. a causal
relationship between low HDL levels and accelerated atherogenesis has not yet
been established. Factors which increase plasma LDL concentration or reduce HDL
concentration, with a consequent increase in the theoretical risk of coronary
atherosclerosis, include obesity, physical inactivity, cigarette smoking, and
progestin-containing oral contraceptives. Recent reports have added to this list
widely used antihypertensive agents, such as thiazide diuretics and
beta-blocking agents. The mechanisms and pathophysiologic significance of such
drug-induced changes in lipoprotein levels are not clear. Until more information
is available, however, it would seem prudent to avoid, whenever possible, any
antihypertensive which in a given patient substantially lowers the HDL/LDL
ratio.
- Language of Publication
- English
- Unique Identifier
- 82218274
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document
- MeSH Heading (Major)
- Coronary Disease|*BL/ET; Lipoproteins|*BL
- MeSH Heading
- Adult; Aged; Antihypertensive Agents|AE; Cholesterol|BL; Female; Human;
Lipoproteins, HDL|BL; Lipoproteins, LDL|BL; Male; Middle Age; Risk; Smoking
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0160-2446
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antihypertensive Agents); 0 (Lipoproteins); 0 (Lipoproteins, HDL
Cholesterol); 0 (Lipoproteins, HDL); 0 (Lipoproteins, LDL Cholesterol); 57-88-5
(Cholesterol)
Record 80 from database: MEDLINE
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- Title
- Biochemical controls of liver cholesterol biosynthesis.
- Author
- Ott DB; Lachance PA
- Address
-
- Source
- Am J Clin Nutr, 1981 Oct, 34:10, 2295-306
- Abstract
- Major endogenous regulatory controls of cholesterol synthesis including
dietary-feedback inhibition, circadian rhythms, feeding/fasting fluctuations,
and enterohepatic bile acid circulation are discussed in terms of biochemical
control mechanisms of liver cholesterol biosynthesis. Other likely control
mechanisms such as cofactors, enzyme levels, and enzyme activities are noted.
The current state of the biochemical knowledge is very dependent upon integrated
data from one experimental animal - the rat. Inferences and implications in the
human are thus limited.
- Language of Publication
- English
- Unique Identifier
- 82043314
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document
- MeSH Heading (Major)
- Cholesterol|*BI; Liver|EN/*ME
- MeSH Heading
- Acetates|ME; Acetyl Coenzyme A|ME; Acyl Coenzyme A|ME; Allosteric
Regulation|DE; Animal; Bile Acids and Salts|PH; Cells, Cultured; Cholesterol,
Dietary|PD; Circadian Rhythm; Diet; Diphosphates|ME; Enterohepatic Circulation;
Fasting; Feedback; Female; Food; Human; Hydroxymethylglutaryl CoA Reductases|ME;
Lipoproteins, LDL|PD; Male; Meglutol|AA/ME; Mevalonic Acid|ME; Rats; Receptors,
Cell Surface|ME; Squalene|ME; Support, Non-U.S. Gov't; Tretinoin|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9165
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 1.1.1.88 (Hydroxymethylglutaryl CoA Reductases); 0 (Acetates); 0 (Acyl
Coenzyme A); 0 (Bile Acids and Salts); 0 (Cholesterol, Dietary); 0
(Diphosphates); 0 (Receptors, Cell Surface); 0 (Receptors, LDL); 111-02-4
(Squalene); 150-97-0 (Mevalonic Acid); 1553-55-5
(3-hydroxy-3-methylglutaryl-coenzyme A); 302-79-4 (Tretinoin); 503-49-1
(Meglutol); 57-88-5 (Cholesterol); 72-89-9 (Acetyl Coenzyme A)
Record 81 from database: MEDLINE
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- Title
- Effect of alpha- and beta-blocker therapy on blood lipids: European
experience.
- Author
- Leren P
- Address
-
- Source
- Am J Med, 1984 Feb 27, 76:2A, 67-71
- Abstract
- Although hypertension is a well-established coronary risk factor,
controlled, randomized hypertension drug trials have failed to show a definite
preventive effect on the incidence of coronary heart disease. Possible adverse
metabolic effects, particularly on blood lipids, of some commonly used
antihypertensive drugs have been investigated. During the Oslo Study on the
treatment of mild hypertension, which was not specifically designed to study the
effect on lipids, a decrease in serum high-density lipoprotein cholesterol and
an increase in serum triglycerides was observed with a combination of
propranolol and hydrochlorothiazide. Therefore, special trials were designed
specifically to study the effect of various antihypertensive drugs on blood
lipids. Propranolol reduced serum high-density lipoprotein cholesterol (13
percent) and the cholesterol ratio [high-density lipoprotein
cholesterol:(low-density lipoprotein cholesterol plus very low-density
lipoprotein cholesterol)] by 15 percent and increased total serum triglycerides
by 24 percent. Prazosin significantly (p less than 0.01) reduced total serum
cholesterol, (9 percent) low-density lipoprotein cholesterol plus very
low-density lipoprotein cholesterol (10 percent), and total triglycerides (16
percent), whereas the cholesterol ratio increased by 7 percent. The reduction in
high-density lipoprotein cholesterol with propranolol plus prazosin was less
than that with propranolol alone. Pindolol (with a high sympathomimetic
activity) did not significantly change total cholesterol, low-density
lipoprotein cholesterol plus very low-density lipoprotein cholesterol,
high-density lipoprotein cholesterol, or total triglycerides. Prazosin plus
pindolol reduced serum low-density lipoprotein cholesterol plus very low-density
lipoprotein cholesterol. The observed reductions in serum high-density
lipoprotein cholesterol and the cholesterol ratio with oxprenolol were 11.5
percent and 13.7 percent, respectively, and with atenolol 16.7 percent and 19.2
percent, respectively, whereas total serum triglycerides were increased by 14.9
percent with oxprenolol and 17.9 percent with atenolol. Data provided by other
European groups comparing the effect of antihypertensive treatment on lipid
metabolism are also reviewed.
- Language of Publication
- English
- Unique Identifier
- 84150895
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document
- MeSH Heading (Major)
- Adrenergic alpha-Antagonists|*TU; Adrenergic beta-Antagonists|*TU;
Hypertension|*DT
- MeSH Heading
- Cholesterol|BL; Comparative Study; Drug Therapy, Combination; Europe; Human;
Male; Middle Age; Norway; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9343
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Adrenergic alpha-Antagonists); 0 (Adrenergic beta-Antagonists); 0
(Triglycerides); 57-88-5 (Cholesterol)
Record 82 from database: MEDLINE
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- Title
- The role of serum high density lipoproteins in adrenal steroidogenesis.
- Author
- Gwynne JT; Hess B; Hughes T; Rountree R; Mahaffee D
- Address
-
- Source
- Endocr Res, 1984-85, 10:3-4, 411-30
- Abstract
- The rat adrenal cortex possesses at least two mechanisms for uptake of
extracellular lipoprotein cholesterol; one is receptor mediated endocytosis and
the second is a non-endocytotic pathway. The latter was revealed by the ability
of lipoproteins such as HDL which do not possess apo B or apo E to enhance
steroid hormone output. Rat adrenocortical cell uptake of HDL cholesterol is
saturable and differs for unesterified cholesterol and cholesterol esters. In
addition rat adrenocortical cells possess ACTH regulated HDL binding sites
although the relationship of HDL receptor activity to cholesterol uptake remains
uncertain. Further elucidation of the "HDL pathway" in the rat adrenal
cortex may have biologic significance beyond understanding adrenal function
since many non-steroidogenic tissues also possess HDL receptors and in man
circulating levels of HDL-cholesterol are a strong inverse risk factor for
accelerated atherosclerosis.
- Language of Publication
- English
- Unique Identifier
- 85257321
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document
- MeSH Heading (Major)
- Adrenal Cortex|DE/*ME; Lipoproteins, HDL|*ME/PD; Steroids|*BI
- MeSH Heading
- Animal; Cholesterol|ME; Cholesterol Esters|ME; Corticotropin|PD; Human; In
Vitro; Lipoproteins, HDL Cholesterol|ME; Lipoproteins, LDL|PD; Mice; Rats;
Receptors, Cell Surface|ME; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0743-5800
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol Esters); 0 (HDL receptor); 0 (Lipoproteins, HDL Cholesterol);
0 (Lipoproteins, HDL); 0 (Receptors, Cell Surface); 0 (Steroids); 57-88-5
(Cholesterol); 9002-60-2 (Corticotropin)
Record 83 from database: MEDLINE
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- Title
- Regulation of cholesterol metabolism in man and in other species.
- Author
- Dietschy JM
- Address
-
- Source
- Klin Wochenschr, 1984 Apr 16, 62:8, 338-45
- Abstract
- In the whole animal and in man, cholesterol is acquired either by absorption
from the diet or by synthesis in the various organs. While there are marked
variations among different animal species, the liver and intestine are generally
the most important organs for the synthesis of cholesterol, although recent data
indicate that nearly all of the remaining tissues of the body also are capable
of significant cholesterol synthesis. Peripheral tissues also acquire
cholesterol through the uptake of low density lipoproteins (LDL). However, most
LDL are removed from the plasma by the liver, and more than 90% of this
clearance process is mediated by the LDL receptor. Hence, the circulating levels
of cholesterol carried in LDL are determined primarily by the rate of LDL
production and the rate of LDL uptake by the liver. Changes in the rate of entry
of cholesterol into the body are compensated for primarily by changes in the
rate of cholesterol synthesis in the liver and, to some extent, in the
intestine. As long as these changes in synthetic rates can fully compensate for
the variations in the rate of cholesterol entry into or exit from the body, the
rate of LDL uptake by the liver and the intestine, and the circulating levels of
plasma cholesterol, remain essentially constant. When the adaptive changes in
cholesterol synthesis are not adequate to meet the changes in cholesterol entry
or exit, then the level of LDL receptor activity in the liver may either
increase or decrease, resulting in a corresponding lowering or elevation of the
circulating plasma LDL-cholesterol levels.
- Language of Publication
- English
- Unique Identifier
- 84217592
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document
- MeSH Heading (Major)
- Cholesterol|AN/BI/*ME
- MeSH Heading
- Acetyl Coenzyme A|ME; Animal; Biological Transport; Endocytosis; Feces|AN;
Hamsters; Human; Liver|ME; Rabbits; Rats; Receptors, Cell Surface|ME; Support,
Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Tritium|DU
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0023-2173
- Country of Publication
- GERMANY, WEST
- CAS Registry/EC Number
- 0 (Receptors, Cell Surface); 0 (Receptors, LDL); 10028-17-8 (Tritium);
57-88-5 (Cholesterol); 72-89-9 (Acetyl Coenzyme A)
Record 84 from database: MEDLINE
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- Title
- The role of lipoprotein receptors in lipid transport and in the pathogenesis
of the hyperlipoproteinemias.
- Author
- Chait A
- Address
-
- Source
- Spec Top Endocrinol Metab, 1983, 5:, 1-53
- Abstract
- Three distinct classes of receptors for lipoproteins exist. The best studied
is the LDL receptor, the primary function of which is the delivery of
cholesterol in response to cellular needs. Although originally thought to be
specific for LDL, it clearly recognizes lipoproteins that contain either apo B
or E. It plays an important role in the catabolism of LDL and could also be
involved in reverse cholesterol transport. The hepatic remnant receptor, a
distinct binding site on liver membranes that recognizes apo E but not apo B,
appears to function in the clearance of chylomicrons (and probably VLDL)
remnants from the circulation, but also is likely to be important in the
recognition of apo E-containing HDL, and hence is likely to participate in the
reverse cholesterol transport. Finally, there is now evidence for a third group
of lipoprotein receptors that are present on the cell surface of macrophages.
They appear to bind lipoproteins that have been altered chemically or
biologically and probably serve a scavenger function. While many of the model
systems for studying these macrophage receptors have focused on chemical
modifications that are unlikely to occur in vivo, several lipoproteins that have
been shown to interact with these receptors may be naturally occurring or result
from biological processes. The discovery of the three receptor classes has
resulted in a dramatic increase in the understanding of lipoprotein physiology
and pathophysiology, and future studies should further expand our understanding
of the regulation of lipoprotein metabolism and its relationship to
hyperlipoproteinemia and atherosclerosis.
- Language of Publication
- English
- Unique Identifier
- 84147458
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document
- MeSH Heading (Major)
- Hyperlipoproteinemia|*ME; Lipids|*ME; Receptors, Cell Surface|ME/*PH
- MeSH Heading
- Animal; Apolipoproteins|ME; Atherosclerosis|ME; Cells, Cultured;
Cholesterol|ME; Chylomicrons|ME; Fibroblasts|ME; Human; Lipoproteins, VLDL|ME;
Liver|ME; Macrophages|ME; Rats
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0193-0982
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins B); 0 (Apolipoproteins E); 0 (Apolipoproteins); 0
(Chylomicrons); 0 (Lipoproteins, VLDL); 0 (Receptors, Cell Surface); 0
(Receptors, Lipoprotein); 0 (Receptors, LDL); 57-88-5 (Cholesterol)
Record 85 from database: MEDLINE
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- Title
- The transport of cholesterol through the plasma in normal man.
- Author
- Myant NB
- Address
-
- Source
- Boll Soc Ital Biol Sper, 1983 Sep 30, 59:9 (Pt 2), 51-100
- Abstract
- This review includes a brief account of the routes of entry of cholesterol
into the plasma by (a) secretion of lipoproteins and (b) uptake of tissue free
cholesterol by lipoproteins in the interstitial fluid, the metabolic
transformation undergone by cholesterol within the plasma, with particular
reference to the esterification of plasma free cholesterol by
lecithin:cholesteryl acyltransferase and the redistribution of esterified
cholesterol from high-density to low-density and very-low-density lipoprotein,
and the routes by which cholesterol is removed from the plasma by bulk
transport. The review end with a balance sheet showing the approximate amounts
of cholesterol entering and leaving the plasma by different routes.
- Language of Publication
- English
- Unique Identifier
- 84052919
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document
- MeSH Heading (Major)
- Cholesterol|*BL
- MeSH Heading
- Animal; Bile Acids and Salts|ME; Biological Transport, Active; Cholesterol
Acyltransferase|ME; Human; Hyperlipoproteinemia Type III|BL; Intestines|ME;
Lecithin Acyltransferase|ME; Lipoproteins|BL; Lipoproteins, HDL|BL;
Lipoproteins, LDL|BL; Liver|ME; Models, Biological; Receptors, Cell Surface|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0037-8771
- Country of Publication
- ITALY
- CAS Registry/EC Number
- EC 2.3.1.26 (Cholesterol Acyltransferase); EC 2.3.1.43 (Lecithin
Acyltransferase); 0 (Bile Acids and Salts); 0 (Lipoproteins); 0 (Lipoproteins,
HDL); 0 (Receptors, Cell Surface); 0 (Receptors, LDL); 57-88-5 (Cholesterol)
Record 86 from database: MEDLINE
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- Title
- Development of accelerated atherosclerosis. Concepts derived from cell
biology and animal model studies.
- Author
- Mahley RW
- Address
-
- Source
- Arch Pathol Lab Med, 1983 Aug, 107:8, 393-9
- Abstract
- Atherosclerosis can be defined as a disease process that occurs when the
influx and deposition of cholesterol into the arterial wall exceed the egress of
cholesterol from the arterial wall. This process is characterized by early
deposition of cholesterol in and around arterial wall cells. The cholesterol is
derived from certain types of plasma lipoproteins. While these lipoproteins
deliver cholesterol to the arterial wall cells, other types of plasma
lipoproteins may be capable of removing cholesterol from the cells and
transporting the cholesterol to the liver for excretion from the body. As the
involvement of various lipoproteins in cholesterol influx and egress is better
understood, the mechanisms whereby accelerated atherosclerosis occurs are more
clearly defined. This review considers recent findings related to identification
of lipoproteins capable of delivering cholesterol to cells of the arterial wall
and those capable of removing cholesterol from these cells for transport to the
liver.
- Language of Publication
- English
- Unique Identifier
- 83255717
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document
- MeSH Heading (Major)
- Arteriosclerosis|ET/*ME
- MeSH Heading
- Animal; Aorta|CY; Apolipoproteins|ME; Cholesterol|ME; Cholesterol,
Dietary|ME/PD; Dietary Fats|PD; Disease Models, Animal; Dogs; Fibroblasts|ME;
Foam Cells|ME; Human; Lipoproteins|BL; Lipoproteins, HDL|ME; Lipoproteins,
LDL|ME; Lipoproteins, VLDL|ME; Macrophages|ME; Muscle, Smooth|ME; Rabbits; Rats;
Receptors, Cell Surface|ME; Swine
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0363-0153
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (apolipoprotein E receptor); 0 (Apolipoproteins); 0 (Cholesterol,
Dietary); 0 (Dietary Fats); 0 (Lipoproteins); 0 (Lipoproteins, HDL); 0
(Lipoproteins, VLDL); 0 (Receptors, Cell Surface); 57-88-5 (Cholesterol)
Record 87 from database: MEDLINE
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- Title
- Lipoprotein utilization and cholesterol synthesis by the human fetal adrenal
gland.
- Author
- Carr BR; Simpson ER
- Address
-
- Source
- Endocr Rev, 1981 Summer, 2:3, 306-26
- Abstract
- A model proposed for regulation of steroidogenesis, lipoprotein utilization
and cholesterol metabolism in HFA tissue is presented in Fig 17. We envision
that the role of ACTH and cAMP in steroidogenesis and cholesterol metabolism is
as follows. ACTH binds to specific receptors on the surface of the cells of the
HFA gland and as a consequence, adenylate cyclase is activated, leading to
increased formation of cAMP. cAMP causes activation of protein kinase that
leads, presumably, to phosphorylation of specific proteins. This leads to the
initiation of reactions that give rise to increased activity of key enzymes and
levels of proteins involved in adrenal cholesterol metabolism. Presumably, the
action of ACTH causes an increase in the activity of cholesterol side chain
cleavage, the rate-limiting step in the conversion of cholesterol to steroid
hormones. We suggest that once the mitochondrial cholesterol side-chain cleavage
system is fully activated by ACTH, the supply of cholesterol to the mitochondria
becomes rate-limiting for steroidogenesis. To meet this demand for cholesterol,
a further action of ACTH results in an increase in the number of LDL receptors.
LDL binds to specific receptors on the cell surface that are localized in coated
pits. LDL is internalized by a process of adsorptive endocytosis and the
internalized vesicles fuse with lysosomes and the protein component of LDL is
hydrolyzed by lysosomal proteolytic enzymes to amino acids. The cholesteryl
esters of LDL also are hydrolyzed to give rise to fatty acids and cholesterol.
The liberated cholesterol is available for utilization in the biosynthesis of
steroid hormones and other cellular processes. In addition, ACTH stimulates the
activity of HMG CoA reductase and, thus, the rate of de novo cholesterol
biosynthesis. In this way sufficient cholesterol is obtained to provide for
precursor cholesterol to maintain the high rate of steroid synthesis by the HFA.
HDL is not utilized as a source of cholesterol by the HFA. Because of the rapid
rate of utilization of LDL by the HFA, fetal plasma levels of LDL are low and
the activity of the HFA is a primary determinant of these levels. Thus, in the
case of anencephaly, in which the activity of the adrenal is very low, plasma
levels of LDL are 2--3 times higher than in normal fetuses, whereas plasma HDL
levels are similar. In addition, in the normal neonate plasma LDL levels rise
rapidly after birth, and this event is coincident with the involution of the
fetal zone of the adrenal. The fetal liver is likely to be the major source
ultimately of the LDL-cholesterol utilized by the HFA. Consequently, factors
that regulate cholesterol and lipoprotein synthesis in the fetal liver may, in
turn, affect the steroidogenic activity of the HFA through regulation of the
supply of cholesterol precursor. Thus, if trophic factors for the HFA other than
ACTH exist, an important site of their action might be the fetal liver, rather
than a direct action to influence the rate of synthesis of steroids by the fetal
adrenal.
- Language of Publication
- English
- Unique Identifier
- 82004075
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document
- MeSH Heading (Major)
- Adrenal Glands|DE/EM/*ME; Cholesterol|*BI; Fetus|*ME; Lipoproteins|*ME
- MeSH Heading
- Anencephaly|ME; Corticotropin|PD; Female; Fetal Blood|ME; Human; Infant,
Newborn; Models, Biological; Organ Culture; Pregnancy; Support, U.S. Gov't,
P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0163-769X
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 57-88-5 (Cholesterol); 9002-60-2 (Corticotropin)
Record 88 from database: MEDLINE
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- Title
- Regulation of plasma cholesterol by lipoprotein receptors.
- Author
- Brown MS; Kovanen PT; Goldstein JL
- Address
-
- Source
- Science, 1981 May 8, 212:4495, 628-35
- Abstract
- The lipoprotein transport system holds the key to understanding the
mechanisms by which genes, diet, and hormones interact to regulate the plasma
cholesterol level in man. Crucial components of this system are lipoprotein
receptors in the liver and extrahepatic tissues that mediate the uptake and
degradation of cholesterol-carrying lipoproteins. The number of lipoprotein
receptors, and hence the efficiency of disposal of plasma cholesterol, can be
increased by cholesterol-lowering drugs. Regulation of lipoprotein receptors can
be exploited pharmacologically in the therapy of hypercholesterolemia and
atherosclerosis is man.
- Language of Publication
- English
- Unique Identifier
- 81177056
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Lipoproteins|*ME; Liver|*ME; Receptors, Cell Surface|ME/*PH
- MeSH Heading
- Atherosclerosis|ME; Biological Transport; Chylomicrons|ME; Dietary Fats|ME;
Homeostasis; Human; Hypercholesterolemia, Familial|ME; Support, U.S. Gov't,
P.H.S.; Triglycerides|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0036-8075
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Chylomicrons); 0 (Dietary Fats); 0 (Lipoproteins); 0 (Receptors, Cell
Surface); 0 (Receptors, Lipoprotein); 0 (Receptors, LDL); 0 (Triglycerides);
57-88-5 (Cholesterol)
Record 89 from database: MEDLINE
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- Title
- Chemical dissolution of common bile duct stones.
- Author
- Leuschner U; Baumgärtel H
- Address
-
- Source
- Prog Clin Biol Res, 1984, 152:, 193-225
- Abstract
- Dissolution of bile duct calculi is complicated by the facts that about
30-40% of them are pigment stones and the stone cannot be unambiguously
identified by radiography before the start of therapy. Thus it does not appear
logical only to infuse irrigation media that dissolve cholesterol (cholate,
Capmul) but to use solutions that also dissolve calcium bilirubinate. Calcium
bilirubinate is the most important compound in primary pigment stones in the
bile duct. Thin sections of calcium bilirubinate stones can be dissolved in EDTA
4Na. The rate is determined by the temperature, the pH, and the surface tension
of the solution. In vitro experiments showed that cholesterol stones and
composition stones can be dissolved more rapidly by alternating therapy with an
EDTA solution and a Capmul preparation than by monotherapy with glycerol
octanoate, and that bovine pigment stones can also be disaggregated. Since
calcium bilirubinate stones consist up to 20-60% of an organic matrix, a mixture
of glycerol octanoate and EDTA was prepared containing SH-activated papain. It
was possible, by using this mixture, to disaggregate human calcium bilirubinate
stones. The process of dissolution is complex and is not yet understood in
detail. It is supposed that the important steps are the extraction of calcium,
the chemical solution and molecular dispersion of bilirubin and cholesterol, and
the disaggregation of the structure of the stone by surface-active substances.
The irrigation media have but little effect on black pigment stones. Toxicity
studies have shown that cholate, glycerol octanoate, and glycerol octanoate
preparations are locally toxic and can lead to cholangitis and cholecystitis in
animals. EDTA solutions bring about lesser changes. In humans, it has not been
possible to distinguish these inflammatory changes unambiguously from those
found in untreated gallstone patients.
- Language of Publication
- English
- Unique Identifier
- 84298287
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document
- MeSH Heading (Major)
- Common Bile Duct Calculi|*TH
- MeSH Heading
- Aged; Animal; Bile Acids and Salts|TU; Bile Duct Diseases|TH; Bile Pigments;
Chelating Agents|TU; Cholesterol; Comparative Study; Dogs; Drug Combinations;
Drug Therapy, Combination; Edetic Acid|TU; Glycerides|TU; Human; Irrigation;
Middle Age; Palmitic Acids|TU; Rabbits; Solubility
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0361-7742
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 0 (Bile Pigments); 0 (Chelating Agents); 0 (Drug
Combinations); 0 (Glycerides); 0 (Palmitic Acids); 26402-26-6 (monooctanoin);
544-31-0 (palmidrol); 57-88-5 (Cholesterol); 60-00-4 (Edetic Acid)
Record 90 from database: MEDLINE
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- Title
- New concepts about the pathogenesis of atherosclerosis in diabetes mellitus.
- Author
- Colwell JA; Winocour PD; Lopes-Virella M; Halushka PV
- Address
-
- Source
- Am J Med, 1983 Nov 30, 75:5B, 67-80
- Abstract
- New concepts about the pathogenesis of atherosclerosis in diabetes mellitus
are presented. Emphasis is given to alterations of endothelial function, as
indicated by von Willebrand factor activity, prostacyclin release, and
fibrinolytic activity in diabetes mellitus. Previous work on platelet
aggregation and arachidonic acid metabolism is updated and recent findings are
emphasized. The atherogenic mix of elevated low-density lipoprotein cholesterol
and low high-density lipoprotein cholesterol levels in uncontrolled diabetes
mellitus is noted. The lipid hypothesis is extended by consideration of very
low-density lipoprotein and intermediate-density lipoprotein metabolism in
diabetes. Lipoprotein-cell interactions that may contribute to atherosclerosis
are reviewed and suggestions are made for future research in order to clarify
the pathogenesis of atherosclerosis in diabetes mellitus.
- Language of Publication
- English
- Unique Identifier
- 84175994
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document
- MeSH Heading (Major)
- Arteriosclerosis|*ET; Atherosclerosis|*ET; Diabetic Angiopathies|*ET
- MeSH Heading
- von Willebrand Factor|AN; Animal; Arachidonic Acids|ME; Blood Platelets|ME;
Cholesterol|ME; Diabetes Mellitus|ME; Endothelium|ME; Epoprostenol|ME;
Fibrinolysis; Human; Lipoproteins|ME; Lipoproteins, HDL|ME; Lipoproteins,
LDL|ME; Lipoproteins, VLDL|ME; Plasminogen Activators|ME; Platelet Aggregation;
Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't,
P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9343
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 3.4.21.- (Plasminogen Activators); 0 (lipoproteins, IDL); 0 (von
Willebrand Factor); 0 (Arachidonic Acids); 0 (Lipoproteins); 0 (Lipoproteins,
HDL Cholesterol); 0 (Lipoproteins, HDL); 0 (Lipoproteins, LDL Cholesterol); 0
(Lipoproteins, VLDL); 35121-78-9 (Epoprostenol); 506-32-1 (Arachidonic Acid);
57-88-5 (Cholesterol)
Record 91 from database: MEDLINE
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- Title
- Clinical and experimental methods for the determination of cholesterol
absorption.
- Author
- Gibson JC
- Address
-
- Source
- Lab Res Methods Biol Med, 1984, 10:, 157-90
- Abstract
- The following section summarizes this methodological treatment of
cholesterol absorption by considering the advantages and disadvantages of the
available methods. As outlined in Table 6, there are certain technical and
interpretational disadvantages to all methods which should be weighed in
deciding the appropriate method to use for a given experimental protocol. Direct
methods are virtually the only ones capable of measuring the total flux of
cholesterol between intestinal lumen and lymph. All the other methods allow
interpretations relating only to the flux of exogenous cholesterol. On the other
hand, the direct methods are invasive--involving surgery--in the case of
experimental animals, and intubation, in the case of intestinal perfusion. This
could potentially lead to unnatural conditions for the absorptive surface of the
gut. Direct methods, balance methods, and the isotopic equilibrium method all
measure a mass of cholesterol transferred. Method IV, the plasma isotope ratio
method, and the continuous feeding method, on the other hand, only provide an
estimate of the percent of an administered dose absorbed, although this can be
converted to a mass estimate with an accurate knowledge of intake. The balance
methods, continuous feeding, and isotopic equilibrium method all provide an
estimate of absorption over time. The plasma isotope ratio method and method IV,
however, rely on repeated measurements to measure fluctuations in absorption. In
their favor, method IV and the isotope ratio technique have several advantages
that make them the methods of choice for human and large-scale animal studies.
These are simplicity, low isotope dosage, and the fact that they are readily
done on an outpatient basis. In general, then, direct or balance methods are
preferable for precise studies where absolute levels of absorbed cholesterol and
fluctuations over time need to be assessed. Direct methods certainly provide the
greatest interpretational flexibility in this regard by measuring endogenous and
exogenous flux. Among balance methods, method II may be the most precise, but
method I is the easiest to perform technically, may be used on an outpatient
basis, and requires lower isotope dosage. For evaluating differences in percent
cholesterol absorption in man and in all animals except the rabbit, the plasma
isotope ratio technique is technically the easiest method both for the
investigator and the subject. It also appears to compare very favorably with the
more tedious balance methods and will undoubtedly be used in more and more
experimental studies of cholesterol absorption.
- Language of Publication
- English
- Unique Identifier
- 85060160
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document
- MeSH Heading (Major)
- Cholesterol|BL/*ME; Intestinal Absorption|*
- MeSH Heading
- Animal; Feces|AN; Human; Mathematics; Methods; Models, Biological;
Radioisotope Dilution Technique; Species Specificity
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0160-8584
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 92 from database: MEDLINE
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- Title
- Mevinolin stimulates receptor-mediated clearance of low density lipoprotein
from plasma in familial hypercholesterolemia heterozygotes.
- Author
- Bilheimer DW; Grundy SM; Brown MS; Goldstein JL
- Address
-
- Source
- Trans Assoc Am Physicians, 1983, 96:, 1-9
- Abstract
- The current results show that one can exploit the normal regulation of
receptor synthesis to stimulate the single normal gene in FH heterozygotes to
produce an increased number of LDL receptors. This stimulation can be achieved
by drugs that inhibit HMG CoA reductase in the liver and by maneuvers that cause
bile acid depletion. These two therapeutic approaches are most effective when
they are combined. It seems reasonable to speculate that such a profound
lowering of plasma cholesterol levels will minimize the development of
atherosclerosis in FH heterozygotes. In a broader sense, the success of this
regulatory manipulation raises the possibility that other genetic diseases may
be treated through manipulation of regulatory signals that control the rates of
synthesis of gene products.
- Language of Publication
- English
- Unique Identifier
- 85041661
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document
- MeSH Heading (Major)
- Anticholesteremic Agents|PD/*TU; Hypercholesterolemia,
Familial|BL/*DT/GE/SU; Lipoproteins, LDL|*BL; Naphthalenes|PD/*TU; Receptors,
LDL|*BI
- MeSH Heading
- Animal; Cholesterol|BI; Colestipol|TU; Combined Modality Therapy; Dogs; Drug
Therapy, Combination; Heterozygote; Human; Ileum|SU; Lipoproteins, LDL
Cholesterol|BL; Liver|ME; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0066-9458
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Anticholesteremic Agents); 0 (Lipoproteins, LDL Cholesterol); 0
(Naphthalenes); 0 (Receptors, LDL); 50925-79-6 (Colestipol); 57-88-5
(Cholesterol); 75330-75-5 (Lovastatin)
Record 93 from database: MEDLINE
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- Title
- Dietary and endogenous cholesterol and human cancer.
- Author
- McMichael AJ; Jensen OM; Parkin DM; Zaridze DG
- Address
-
- Source
- Epidemiol Rev, 1984, 6:, 192-216
- Abstract
- Recent questions about the role of cholesterol (particularly blood
cholesterol) in human cancer have assumed considerable scientific and public
health importance. This paper has reviewed the evidence relating human cancer to
cholesterol, in diet, blood, and feces. With respect to dietary cholesterol,
there is moderately consistent evidence, both descriptive and analytic, of a
small-to-medium increase in risk of cancers of the colon and female breast in
association with increased dietary cholesterol. However, the close correlation
of cholesterol with other foods and nutrients precludes causal inference. The
association of fecal cholesterol with large bowel cancer, in both descriptive
and analytic studies, is inconsistent. However, there is some evidence that
individuals with reduced degradation of fecal cholesterol are at increased risk
of colon cancer. Other bile-derived fecal components, particularly the acid
sterols, show a somewhat more consistent relationship with large bowel cancer.
It may be of relevance to the findings on blood cholesterol that bile is
produced from hepatic cholesterol which derives, in part, from blood
cholesterol. Studies of blood cholesterol and cancer have been either
experimental (intervention) or observational (primarily follow-up). Deliberate
lowering of blood cholesterol, by either drugs or diet, does not appear to alter
the risk of cancer, either overall or of specific types. The findings from 20
published follow-up studies, each initiated as a cardiovascular disease study,
have been more varied. In 12 studies, an inverse association was observed
between blood cholesterol level and overall cancer risk. Eight of those 12 were
mortality studies, and in six, the inverse association was confined to deaths
that occurred early in follow-up; this observation is consistent with lowered
blood cholesterol having occurred as a metabolic response to a preclinical
cancer. However, the results of the other two mortality studies do not
exclusively support this interpretation. Furthermore, in three of the four
incidence studies that reported an inverse association, the inverse association
persisted for 10 or more years. This relationship was most marked for colon
cancer in men and showed some evidence of being maximal in the proximal colon.
The biologic plausibility of these particular observations on colon cancer risk
in relationship to an antecedent naturally occurring low blood cholesterol gains
some support from a body of epidemiologic, clinical, and experimental
evidence.(ABSTRACT TRUNCATED AT 400 WORDS)
- Language of Publication
- English
- Unique Identifier
- 85027587
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document
- MeSH Heading (Major)
- Cholesterol|*BL/ME; Cholesterol, Dietary|*AE/ME; Neoplasms|*BL
- MeSH Heading
- Adult; Age Factors; Aged; Animal; Anticholesteremic Agents|TU; Breast
Neoplasms|BL; Clinical Trials; Colonic Neoplasms|BL/CI; Diet;
Dimethylhydrazines; Epidemiologic Methods; Feces|AN; Female; Human; Male; Mice;
Middle Age; Neoplasms, Experimental|CI; Precancerous Conditions|BL; Prospective
Studies; Rats; Risk; Sex Factors
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW
- ISSN
- 0193-936X
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Anticholesteremic Agents); 0 (Cholesterol, Dietary); 0
(Dimethylhydrazines); 57-88-5 (Cholesterol)
Record 94 from database: MEDLINE
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- Title
- Plasma lipid transport.
- Author
- Spector AA
- Address
-
- Source
- Clin Physiol Biochem, 1984, 2:2-3, 123-34
- Abstract
- The main plasma lipid transport forms are free fatty acid, triglyceride and
cholesteryl ester. Free fatty acid, derived primarily from adipocyte
triglycerides, is transported as a physical complex with plasma albumin.
Triglycerides and cholesteryl esters are transported in the core of plasma
lipoproteins. The intestine secretes dietary fat in chylomicrons, lipoproteins
that transport triglyceride to tissues for storage. Dietary cholesterol is
transported to the liver by chylomicron remnants which are formed from
chylomicrons. Triglyceride is released from the liver in very low density
lipoproteins for utilization and storage in extrahepatic tissues. Very low
density lipoproteins are converted to low density lipoproteins in the plasma; in
the process, they become enriched in cholesteryl esters. High density
lipoproteins take up cholesterol from tissues and other plasma lipoproteins.
After the cholesterol is esterified, it is transferred ultimately to low density
lipoproteins for uptake by the tissues. Phospholipids are structural components
of lipoproteins and provide fatty acid for cholesteryl ester formation in the
plasma, but they are not a primary transport form of lipid. Six enzymes,
together with apolipoprotein cofactors and lipid transfer proteins, facilitate
the plasma lipid transport process.
- Language of Publication
- English
- Unique Identifier
- 85025749
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document
- MeSH Heading (Major)
- Lipids|*BL
- MeSH Heading
- Albumins|ME; Biological Transport, Active; Cholesterol|BL/ME; Cholesterol
Esters|BL/ME; Fatty Acids|BL; Fatty Acids, Nonesterified|BL/ME; Human;
Intestines|ME; Liver|ME; Phospholipids|BL/ME; Support, U.S. Gov't, P.H.S.;
Triglycerides|BL/ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0252-1164
- Country of Publication
- SWITZERLAND
- CAS Registry/EC Number
- 0 (Albumins); 0 (Cholesterol Esters); 0 (Fatty Acids); 0 (Fatty Acids,
Nonesterified); 0 (Phospholipids); 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 95 from database: MEDLINE
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- Title
- Cholesterol and cardiovascular disease. An overview of Lipid Research
Clinics (LRC) epidemiologic studies as background for the LRC Coronary Primary
Prevention Trial.
- Author
- Tyroler HA
- Address
-
- Source
- Am J Cardiol, 1984 Aug 27, 54:5, 14C-19C
- Abstract
- The Lipid Research Clinics (LRC) Program has implemented an integrated
series of observational epidemiologic, community-based studies that provide a
frame of reference for the results of the LRC Coronary Primary Prevention Trial
(CPPT). The observational studies were performed in 16 populations sampled in
the United States, Canada, the Soviet Union and Israel. Findings based on data
from more than 80,000 study participants indicate that atherogenic profiles of
plasma total, low-density lipoprotein and high-density lipoprotein cholesterol
levels are highly prevalent in middle-aged adults. The lipoprotein cholesterol
fraction components are related to a wide range of demographic, behavioral,
anthropometric, medical status, drug utilization and hormonal factors, in
addition to the well known major dietary and genetic determinants. The results
of the LRC CPPT are directly applicable to high-risk, high total cholesterol,
and high low-density lipoprotein cholesterol levels in middle-aged men.
Considered jointly with the observational finding that the major burden of
ischemic heart disease is associated with moderately elevated lipid levels, the
LRC studies suggest that 2 concurrent approaches are necessary to achieve
community control: approaches for high-risk person through individualized
medical intervention and hygienic, population-oriented approaches toward
achieving less atherogenic distributions of lipids and lipoproteins. With this
combined approach, the current epidemic of ischemic heart disease can be
controlled.
- Language of Publication
- English
- Unique Identifier
- 84303890
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|BL/EP/*PC; Primary Prevention|*
- MeSH Heading
- Adolescence; Adult; Aged; Canada; Clinical Trials; Estrogens|AD; Female;
Human; Israel; Lipoproteins, HDL|BL; Lipoproteins, LDL|BL; Male; Menopause;
Middle Age; United States; USSR
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Estrogens); 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL); 0
(Lipoproteins, LDL Cholesterol); 57-88-5 (Cholesterol)
Record 96 from database: MEDLINE
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- Title
- Pathogenesis of gallstones.
- Author
- Weisberg HF
- Address
-
- Source
- Ann Clin Lab Sci, 1984 Jul-Aug, 14:4, 243-51
- Abstract
- The three lipids in bile, cholesterol, lecithin, and bile salts (about 90
percent of the dry weight of normal gallbladder bile) are amphipathic substances
having both hydrophobic and hydrophilic functional groups. Knowledge of the
physicochemical factors of gallstone formation (especially cholesterol stones)
has increased in the past two decades. The absolute amount of cholesterol
supersaturation determines the extent of cholesterol precipitation. The ionic
strength of the bile and the types of bile salts present are minor factors,
whereas the ratios of bile salts to lecithin at a particular concentration of
total lipids are the major factors contributing to gallstone production. Bile
acids (salts) form micelles which allow the lecithin and cholesterol to dissolve
within the micelles. Thus the administration of bile acids allows for
non-invasive dissolution of some cholesterol gallstones. Additional important
risk factors are genetic and ethnic, sex (females predominate), obesity, diet
(in contrast to animal protein and more refined carbohydrate diets, there is
less lithogenicity with diets containing plant protein and unrefined
carbohydrates), certain diseases, and drug therapy. Pigment stones make up the
majority of radiopaque stones and are predominant in the Orient; they are seen
in certain diseases and in infections of the biliary tree.
- Language of Publication
- English
- Unique Identifier
- 84278841
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document
- MeSH Heading (Major)
- Bile|*AN/PH; Cholelithiasis|*ET/GE/ME; Cholesterol|*AN/ME; Lipids|*AN
- MeSH Heading
- Animal; Bile Acids and Salts|AN; Bile Duct Diseases|CO; Diet|AE; Ethnic
Groups; Female; History of Medicine, Ancient; History of Medicine, 16th Cent.;
Human; Obesity|CO; Phosphatidylcholines|AN; Phospholipids|AN; Pregnancy; Risk;
Sex Factors
- Publication Type
- HISTORICAL ARTICLE; JOURNAL ARTICLE; REVIEW
- ISSN
- 0091-7370
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 0 (Phosphatidylcholines); 0 (Phospholipids);
57-88-5 (Cholesterol)
Record 97 from database: MEDLINE
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- Title
- The influence of exercise on the concentrations of triglyceride and
cholesterol in human plasma.
- Author
- Haskell WL
- Address
-
- Source
- Exerc Sport Sci Rev, 1984, 12:, 205-44
- Abstract
- Exercise exerts both acute and chronic effects on plasma lipid and
lipoprotein concentrations. Much of the triglyceride-lowering effect is an acute
response, with the changes in cholesterol having a greater chronic component.
The acute Tg decrease seems to be due to accelerated catabolism resulting from
increased LPL activity. Following exercise, and on a more chronic basis,
decreased VLDL-Tg synthesis may also occur in response to an increase in tissue
insulin sensitivity. The low body fat content of endurance-trained athletes also
contributes to lower Tg concentrations, through this same mechanism. The
magnitude of the plasma Tg response to acute or chronic exercise is highly
influenced by preexercise values--decreases in plasma Tg occur only when
preexercise values are elevated. The major exercise effect on plasma cholesterol
appears to be an increase in HDL-C as a result of endurance training, very
likely related to the increase in LPL activity and Tg catabolism. This response
is not always achieved with exercise training, and has been especially difficult
to demonstrate in previously sedentary women. Exercise effects on HDL-C may be
augmented by weight loss or changes in nutrient intake, but these
interrelationships are not well established. A dose-response relationship
exists, with the lower threshold influenced by baseline HDL-C values and
exercise status. The higher HDL-C associated with endurance training is the
result of increases in the less dense HDL2 subfraction, with elevations in both
the lipid and protein components. Relatively small decreases in LDL-C occur with
training. The biological mechanisms for these exercise effects have not been
established.
- Language of Publication
- English
- Unique Identifier
- 84236310
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Exertion|*; Triglycerides|*BL
- MeSH Heading
- Adolescence; Adult; Age Factors; Aged; Chylomicrons|BL; Coronary Disease|PP;
Female; Human; Hyperlipidemia|PP; Lipoprotein Lipase|ME; Lipoproteins, HDL|BL;
Lipoproteins, LDL|BL; Lipoproteins, VLDL|BL; Male; Middle Age; Muscles|EN;
Physical Education and Training; Physical Endurance; Sex Factors; Time Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0091-6331
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 3.1.1.34 (Lipoprotein Lipase); 0 (Chylomicrons); 0 (Lipoproteins, HDL
Cholesterol); 0 (Lipoproteins, HDL); 0 (Lipoproteins, LDL Cholesterol); 0
(Lipoproteins, VLDL); 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 98 from database: MEDLINE
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- Title
- Risk factors for coronary heart disease--assessment in airline pilots.
- Author
- Lewis B
- Address
-
- Source
- Eur Heart J, 1984 Mar, 5 Suppl A:, 17-24
- Abstract
- Biochemical risk factors have a potent impact on the overall risk in the
development of coronary heart disease (CHD). This impact is greater in men and
in women after the menopause. The prevalence of familial hypercholesterolaemia
(Familial Type IIa) in the U.K. is approximately 2.5/1000, and 50% of affected
males develop overt CHD by the age of 50. The prevalence of Type III
hyperlipoproteinaemia is lower. More minor elevations of the plasma cholesterol
in association with smoking and/or hypertension, however, may confer a similar
overall risk of CHD. Usually minor adverse biochemical effects may be produced
by treatment with antihypertensive agents. It is suggested that measurement of
fasting cholesterol, including the HDL fraction, together with triglyceride and
glucose in new applicants for medical certificates to fly, will identify a small
subset at high risk for the development of CHD. Repeat studies at intervals
would then be needed. The presence of abnormalities in the plasma lipids
associated with excessive smoking and/or minor hypertension make a reasonable
case for denying a single-crew certification.
- Language of Publication
- English
- Unique Identifier
- 84208094
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document
- MeSH Heading (Major)
- Aerospace Medicine|*; Coronary Disease|ET/*PC; Hypercholesterolemia,
Familial|*DI; Hyperlipoproteinemia Type III|*DI; Personnel Management|*MT;
Personnel Selection|*MT
- MeSH Heading
- Adult; Cholesterol|BL; Comparative Study; Female; Human; Lipoproteins,
HDL|BL; Lipoproteins, LDL|BL; Lipoproteins, VLDL|BL; Male; Middle Age; Risk;
Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0195-668X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL); 0 (Lipoproteins,
LDL Cholesterol); 0 (Lipoproteins, VLDL Cholesterol); 0 (Lipoproteins, VLDL); 0
(Triglycerides); 57-88-5 (Cholesterol)
Record 99 from database: MEDLINE
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- Title
- Adipose tissue and cholesterol metabolism.
- Author
- Krause BR; Hartman AD
- Address
-
- Source
- J Lipid Res, 1984 Feb, 25:2, 97-110
- Abstract
- Adipose tissue in man is a major site for cholesterol storage. In obesity
over half of total body cholesterol may reside within this tissue; however,
relatively little attention has been directed toward understanding the
cholesterol metabolism and its relationship to whole body cholesterol
homeostasis in this tissue. In this review the factors which influence
cholesterol storage are discussed, with particular emphasis on the effects of
diet and drug treatment in both animals and man. The uptake, synthesis, and
mobilization of adipose tissue cholesterol appears to be mediated and/or
regulated, as in other tissues, by the plasma lipoproteins, and these processes
are examined with regard to both normal and pathologic states.
- Language of Publication
- English
- Unique Identifier
- 84163637
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document
- MeSH Heading (Major)
- Adipose Tissue|*ME; Cholesterol|BI/*ME
- MeSH Heading
- Age Factors; Animal; Antilipemic Agents|PD; Apolipoproteins|ME; Body Weight;
Cardiovascular Diseases|ME; Cholesterol Esterase|ME; Dietary Fats|ME; Fats,
Unsaturated|ME; Human; Hypercholesterolemia|ME; Lipoproteins|ME; Rabbits; Rats;
Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0022-2275
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 3.1.1.13 (Cholesterol Esterase); 0 (Antilipemic Agents); 0
(Apolipoproteins); 0 (Dietary Fats); 0 (Fats, Unsaturated); 0 (Lipoproteins);
57-88-5 (Cholesterol)
Record 100 from database: MEDLINE
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- Title
- Transport of cholesterol.
- Author
- Norum KR; Berg T; Helgerud P; Drevon CA
- Address
-
- Source
- Physiol Rev, 1983 Oct, 63:4, 1343-419
- Abstract
- .ur current model for cholesterol transport is summarized in Figure 10. In
this figure we have put together the various steps in cholesterol transport that
were described previously in this review. Under normal conditions, cholesterol
metabolism and transport are well regulated. If the transport system is
overloaded for a long time, however, hypercholesterolemia caused mainly by
increased plasma LDL may develop in several species, including humans. Under
such circumstances reverse transport of cholesterol may also fail, giving rise
to deposits of cholesterol. Tissue macrophages may be responsible for this lipid
accumulation, because receptor-mediated (adsorptive) endocytosis of
lipoprotein-associated cholesterol in these cells is not under negative-feedback
control. The deposits are mainly found in tissues poorly supplied with blood and
lymph: the skin, tendons, the cornea, and arteries. Overload of cholesterol
transport may be the result of too much fat and cholesterol in the diet, giving
rise to cholesterol-rich lipoproteins from the gut and to increased production
of liver (formula; see text) VLDL, which in humans ends up as LDL. In many
individuals, however, no hypercholesterolemia is seen, even after eating large
amounts of a "western" diet for decades; others may develop increased
LDL on a relatively "prudent" diet. Obviously many of the factors and
mechanisms in cholesterol transport are influenced by genetic factors. Although
studies of several inborn errors of lipid metabolism have given information
about some mechanisms, the quantitatively more important differences in genetic
patterns, which determine whether or not a western diet will result in
hyperlipidemia, are not well known. Perhaps studies of different forms of apoB
and apoE and of HDL subgroups and hyper-alpha-lipoproteinemia will explain why
certain individuals develop hypercholesterolemia and premature atherosclerosis.
All the recent information related to cholesterol metabolism and transport gives
rise to new questions. There are many problems of interest for future research:
What are the metabolic differences between the apoB produced in the liver and
that produced in the gut? To what extent is the protein moiety of LDL modified
in the plasma of blood and lymph and in interstitial tissue? Are such
modifications important to whether LDL uptake goes through the classic LDL
pathway or through the macrophage (i.e., scavenger?) pathway? Are some changes
in apoB important for liver recognition of LDL?(ABSTRACT TRUNCATED AT 400 WORDS)
- Language of Publication
- English
- Unique Identifier
- 84095898
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document
- MeSH Heading (Major)
- Cholesterol|BL/*ME/PH
- MeSH Heading
- Animal; Biological Transport; Blood Vessels|ME; Cholesterol
Acyltransferase|ME; Cholesterol Esterase|ME; Cholesterol Esters|BL/PH; Human;
Intestine, Small|ME; Lecithin Acyltransferase|ME; Lipoproteins|BI/ME; Liver|ME;
Membrane Lipids|PH; Models, Biological; Support, Non-U.S. Gov't;
Triglycerides|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0031-9333
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 2.3.1.26 (Cholesterol Acyltransferase); EC 2.3.1.43 (Lecithin
Acyltransferase); EC 3.1.1.13 (Cholesterol Esterase); 0 (Cholesterol Esters); 0
(Lipoproteins); 0 (Membrane Lipids); 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 101 from database: MEDLINE
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- Title
- Regulation and interaction of cholesterol, bile salt and lipoprotein
synthesis in liver.
- Author
- Barth CA
- Address
-
- Source
- Klin Wochenschr, 1983 Dec 1, 61:23, 1163-70
- Abstract
- The liver is the junction of several inter-organ metabolic cycles which are
essential for the homeostasis of mammalian metabolism. Two of these are
described in greater detail and their role in control of lipid metabolism will
be presented. The fatty acid-triglyceride cycle is of particular importance for
our understanding of the mechanisms governing serum lipid levels. This is due to
the fact that the lipoprotein secreted by the liver in the course of this
metabolic cycle - very low density lipoprotein - has a relatively long half-life
in the plasma compartment. Data have been collected from the literature to show
that different nutritional and pharmacological stimuli affecting serum lipid
levels do so by interfering with the rate of very low density lipoprotein input
into the plasma compartment. The enterohepatic circulation of steroids is
another cycle which contributes to control of lipid metabolism. Data are
presented which show that bile acids, the major steroids circulating in this
cycle, exert direct feedback control of hepatic cholesterol synthesis. This
characteristic of bile acids may explain why certain bile acids, when given
orally, reduce serum cholesterol levels. Several clinical and experimental
observations suggest a close relation between bile acid and triglyceride
metabolism. It is characterized by an inverse relation between bile acid pool
size and serum triglyceride levels. Moreover, a reduction of the bile acid pool
size is accompanied by an enhanced hepatic fatty acid and triglyceride synthesis
and secretion into blood. The molecular basis and physiological significance of
these observations have still to be explored.(ABSTRACT TRUNCATED AT 250 WORDS)
- Language of Publication
- English
- Unique Identifier
- 84091368
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document
- MeSH Heading (Major)
- Bile Acids and Salts|*ME; Cholesterol|*ME; Lipoproteins, VLDL|*BI;
Liver|CY/*ME
- MeSH Heading
- Cells, Cultured; Enterohepatic Circulation; Fatty Acids, Nonesterified|ME;
Human; Hyperlipoproteinemia Type IV|ME; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0023-2173
- Country of Publication
- GERMANY, WEST
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 0 (Fatty Acids, Nonesterified); 0 (Lipoproteins,
VLDL); 57-88-5 (Cholesterol)
Record 102 from database: MEDLINE
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- Title
- Risk factors and atherosclerotic lesions. A review of autopsy studies.
- Author
- Solberg LA; Strong JP
- Address
-
- Source
- Arteriosclerosis, 1983 May-Jun, 3:3, 187-98
- Abstract
- This review assesses the current status of knowledge concerning the
relationship of risk factors to atherosclerotic lesions. Risk factors for
atherosclerotic lesions per se need not necessarily be identical to those
related to clinically overt coronary heart disease (CHD). This review is based
on 1) autopsy studies where information risk factors was gathered in a
retrospective fashion; and 2) autopsy studies where information on risk factors
was gathered prospectively. In spite of differences in study designs and grading
methods among the studies, the general findings were similar. Elevated serum
cholesterol and blood pressure are positively and significantly related to
atherosclerotic lesions. High density lipoprotein cholesterol is inversely
related to coronary and probably also to cerebral atherosclerosis. Almost all
studies indicate a significant association between cigarette smoking and degree
of aortic atherosclerosis; a positive relationship between smoking and coronary
atherosclerosis is found between obesity or physical activity and the degree of
atherosclerosis. Data from the Community Pathology Study in New Orleans indicate
that the average extent of coronary atherosclerosis in a population may be
subject to changes within a relatively short period of time; these changes might
be expected to parallel changes in risk factors in the population.
- Language of Publication
- English
- Unique Identifier
- 83203653
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document
- MeSH Heading (Major)
- Arteriosclerosis|*EP; Atherosclerosis|CO/*EP/PA
- MeSH Heading
- Adult; Aged; Aorta|PA; Autopsy; Cerebral Arteries|PA; Cholesterol|BL;
Coronary Disease|EP; Coronary Vessels|PA; Diabetes Mellitus|CO; Diastole;
Female; Human; Hypertension|CO; Lipoproteins, HDL|BL; Louisiana; Male; Middle
Age; Norway; Risk; Sex Factors; Smoking; Support, U.S. Gov't, P.H.S.; Systole;
Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL); 0 (Triglycerides);
57-88-5 (Cholesterol)
Record 103 from database: MEDLINE
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- Title
- Choice and use of blood lipid tests. An epidemiologic perspective.
- Author
- Hulley SB; Lo B
- Address
-
- Source
- Arch Intern Med, 1983 Apr, 143:4, 667-73
- Abstract
- Serum cholesterol is a useful test in asymptomatic adults who are interested
in preventing coronary heart disease (CHD). It guides the decision to recommend
a fat-controlled diet to reduce the serum cholesterol level; this intervention
probably decreases the risk of CHD in patients with high levels (eg, greater
than 240 mg/dL), but not in those with lower levels (the majority). The
potential effect of such intervention on absolute (attributable) CHD risk is
relatively large in males and in patients with other risk factors. Dietary
intervention probably has less effect on CHD risk than eliminating smoking or
controlling hypertension. Lipid and lipoprotein tests other than cholesterol are
not generally needed, although high-density lipoprotein cholesterol may be
useful in certain situations. These epidemiologic considerations, tempered by
the preferences of the patient, are useful for individualizing preventive
medicine decisions.
- Language of Publication
- English
- Unique Identifier
- 83177246
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|DH/ET/*PC; Lipids|*BL; Lipoproteins,
HDL|*BL; Triglycerides|*BL
- MeSH Heading
- Adult; Age Factors; Aged; Alcohol Drinking; Comparative Study; Decision
Making; Epidemiologic Methods; Female; Human; Male; Middle Age; Obesity;
Physical Fitness; Risk; Sex Factors; Smoking; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0003-9926
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL); 0 (Triglycerides);
57-88-5 (Cholesterol)
Record 104 from database: MEDLINE
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- Title
- Review of the epidemiological evidence for a possible relationship between
hypocholesterolemia and cancer.
- Author
- Feinleib M
- Address
-
- Source
- Cancer Res, 1983 May, 43:5 Suppl, 2503s-2507s
- Abstract
- The evidence relating hypocholesterolemia to an increased risk of cancer is
controversial. Although more than a dozen populations have been studied in
prospective epidemiological investigations, there is relatively little
consistency relating low serum cholesterol levels to future risk or mortality
from cancer. Several studies have demonstrated a significant inverse
relationship, but many others have failed to do so, and there is no ready
explanation for the divergence of results. The data from dietary studies, both
at the group level and at the individual level, indicate that, if anything,
higher intakes of cholesterol appear to be related to cancer rather than lower
levels. A potential role for vitamin A and for some genetic predisposition to
cancer perhaps associated with lower cholesterol absorption and decreased
degradation of cholesterol in the gut may possibly explain some of these
inconsistencies. It is concluded that: (a) the available data do not
substantiate any direct cause and effect relationship between low blood
cholesterol levels and cancer. Rather, the data suggest that low cholesterol
levels may serve as a "marker," possibly genetic, and in only small
numbers of male individuals in any given population; (b) the data do not
preclude, countermand, or contradict the current public health message which
recommends that those with elevated cholesterol levels seek to lower them
through diets lower in saturated fat and cholesterol.
- Language of Publication
- English
- Unique Identifier
- 83155381
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Neoplasms|*ET/MO
- MeSH Heading
- Cholesterol, Dietary; Female; Human; Male; Risk
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0008-5472
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol, Dietary); 57-88-5 (Cholesterol)
Record 105 from database: MEDLINE
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- Title
- Secondary prevention in elderly survivors of heart attacks.
- Author
- Davenport J; Whittaker K
- Address
- Kaiser Permanente Medical Center, Anaheim, California.
- Source
- Am Fam Physician, 1988 Jul, 38:1, 216-24
- Abstract
- More than 200,000 elderly patients survive myocardial infarctions each year.
Thus, the achievement of even minimal decreases in reinfarction and mortality
rates will benefit large numbers of patients. Secondary prevention strategies
include smoking cessation; the control of hyperlipidemia, obesity and diabetes;
the management of hypertension and stress; exercise; the use of drugs such as
beta blockers and aspirin, and increased attention to general health.
- Language of Publication
- English
- Unique Identifier
- 88279324
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document
- MeSH Heading (Major)
- Myocardial Infarction|EP/ET/*PC
- MeSH Heading
- Adrenergic beta-Antagonists|TU; Aged; Aspirin|TU; Cholesterol|BL; Female;
Human; Hypertension|CO; Male; Recurrence; Risk Factors; Smoking|AE
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-838X
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Adrenergic beta-Antagonists); 50-78-2 (Aspirin); 57-88-5 (Cholesterol)
Record 106 from database: MEDLINE
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- Title
- The use of isotopic tracers in studying lipid metabolism in human subjects.
- Author
- Klein S; Wolfe RR
- Address
-
- Source
- Baillieres Clin Endocrinol Metab, 1987 Nov, 1:4, 797-816
- Abstract
- We have attempted to evaluate some of the tracer methodologies involved in
studying lipid metabolism in humans. The magnitude of this subject prohibits a
comprehensive review of all areas. Since the major function of adipose tissue
appears to be to supply the body with energy, we have particularly emphasized
the approaches used to study the mobilization and oxidation of fat. The
importance of these issues, as well as the increasing availability of
non-radioactive tracers, suggest an optimistic future for this area of research.
- Language of Publication
- English
- Unique Identifier
- 88240224
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document
- MeSH Heading (Major)
- Lipids|*ME; Radioisotopes|*DU
- MeSH Heading
- Absorption; Cholesterol|PK; Esterification; Fatty Acids|ME/PK; Human;
Lipolysis; Oxidation-Reduction; Triglycerides|PK
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0950-351X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Fatty Acids); 0 (Radioisotopes); 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 107 from database: MEDLINE
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- Title
- Genetic architecture of inter-individual variability in apolipoprotein,
lipoprotein and lipid phenotypes.
- Author
- Sing CF; Boerwinkle EA
- Address
- Department of Human Genetics, University of Michigan, Ann Arbor 48109-0618.
- Source
- Ciba Found Symp, 1987, 130:, 99-127
- Abstract
- Phenotypes that predict coronary heart disease (CHD) are the consequence of
interactions between many genetic and environmental factors. Quantitative
measures of plasma apolipoproteins, lipoproteins and lipids are examples of
phenotypes that link genetic and environmental factors to the CHD end-point.
Population studies in Hawaii, Michigan and elsewhere have established that a
significant fraction of variability in these phenotypes is attributable to
genetic differences among individuals. Recent advances in molecular biology
provide measures of the gene loci that code for the apolipoproteins, the
cellular receptors for lipoprotein particles and the catalysts and cofactors in
lipoprotein metabolism. By measuring polymorphic protein variability and
restriction site variability in small regions of DNA known to contain genes that
code for the proteins involved in these functions, it is possible to assign
polygenetic effects to specific alleles or haplotypes. This 'measured genotype'
approach may be used to study the genetic architecture (number of loci involved,
the frequencies and effects of their alleles, and the type of loci, i.e.,
structural or regulatory) of quantitative variation in the plasma
apolipoproteins, lipoproteins and lipids. This paper reviews statistical models,
sampling designs and results of studies designed to estimate the genetic
architecture of selected apolipoproteins, lipoproteins and lipids. The
usefulness of these studies for answering questions about the prediction of CHD
in the population, the family and the individual are discussed and the
directions that human quantitative genetic studies will take in the future are
considered.
- Language of Publication
- English
- Unique Identifier
- 88166256
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document
- MeSH Heading (Major)
- Apolipoproteins|*GE; Coronary Disease|*GE; Lipids|*GE; Lipoproteins|*GE
- MeSH Heading
- Cholesterol|GE; Chromosome Mapping; Genotype; Human; Mutation; Phenotype;
Support, U.S. Gov't, P.H.S.; Variation (Genetics)
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0300-5208
- Country of Publication
- NETHERLANDS
- CAS Registry/EC Number
- 0 (Apolipoproteins); 0 (Lipoproteins); 57-88-5 (Cholesterol)
Record 108 from database: MEDLINE
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- Title
- Electrocardiographic abnormalities and coronary heart disease mortality
among hypertensive men in the Multiple Risk Factor Intervention Trial.
- Author
- Rautaharju PM; Neaton JD
- Address
- Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova
Scotia.
- Source
- Clin Invest Med, 1987 Nov, 10:6, 606-15
- Abstract
- The Multiple Risk Factor Intervention Trial (MRFIT) was a primary prevention
trial involving 12,286 middle-aged men at high risk of future heart attack,
about two-thirds of them considered hypertensive at entry. The mortality results
suggested an increased risk of coronary heart disease (CHD) death, particularly
sudden death, possibly associated with hypertension control, following a
stepped-care protocol including diuretics, among hypertensive MRFIT
special-intervention (SI) participants with abnormalities in their rest ECG. No
such adverse association was evident in the usual care (UC) group. ECG data from
the Dalhousie ECG program revealed that for nearly every ECG abnormality
considered, the risk of CHD death for hypertensive SI men was greater than for
hypertensive UC men. The exception to this was ischemic response to exercise,
for which the associated relative risk for UC men was 2.96 and for SI men 1.35
(p = 0.03 for SI/UC difference). The risk of CHD death for SI men with any ECG
abnormalities compared to those without ECG abnormalities was 3.30. For UC men
the corresponding relative risk was 1.22 (p = 0.03 for difference in relative
risk). The results suggest that the influence of the presence of ECG
abnormalities on the response to hypertension intervention may be heterogeneous,
in that certain abnormalities (particularly repolarization abnormalities at
rest, and absent or low-amplitude U waves at rest and in post-exercise ECG) may
be associated with an adverse response or reduced effectiveness of hypertension
intervention, whereas an ischemic ST response to exercise may be associated with
a beneficial response to intensive hypertension control efforts.
- Language of Publication
- English
- Unique Identifier
- 88151301
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document
- MeSH Heading (Major)
- Coronary Disease|BL/*MO/PP; Electrocardiography|*; Hypertension|*CO/PP/TH
- MeSH Heading
- Adult; Cholesterol|BL; Clinical Trials; Comparative Study; Death, Sudden;
Exertion; Human; Male; Middle Age; Random Allocation; Rest; Risk Factors;
Smoking; Support, Non-U.S. Gov't
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE
- ISSN
- 0147-958X
- Country of Publication
- CANADA
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 109 from database: MEDLINE
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- Title
- The yield from work site cardiovascular risk reduction.
- Author
- Leviton LC
- Address
- Department of Health Services Administration, Graduate School of Public
Health, University of Pittsburgh, PA 15261.
- Source
- J Occup Med, 1987 Dec, 29:12, 931-6
- Abstract
- Health decision makers in business need to know what to expect from efforts
at cardiovascular risk reduction offered through the workplace. In terms of
health, the yield from such efforts is the extent to which risk in the entire
work force is lowered. Yield is assessed from available reports of
interventions, and is defined as the joint probability of (1) participation of
the at-risk work force, (2) retention of participants in an intervention, and
(3) improvement on an indicator of risk. The median and range of outcomes are
presented so that decision makers can better know what to expect and can have a
basis of comparison for the performance of their own risk reduction programs.
- Language of Publication
- English
- Unique Identifier
- 88117851
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Hypertension|ET/*PC; Occupational Health Services|*;
Smoking|*PC
- MeSH Heading
- Environmental Exposure; Human; Risk Factors; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0096-1736
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 110 from database: MEDLINE
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- Title
- The epidemiological importance of intraindividual changes in objective
pulmonary responses.
- Author
- Lebowitz MD; Quackenboss J; Camilli AE; Bronnimann D; Holberg CJ; Boyer B
- Address
- Division of Respiratory Sciences, University of Arizona College of Medicine,
Tucson 85724.
- Source
- Eur J Epidemiol, 1987 Dec, 3:4, 390-8
- Abstract
- Debate continues about what constitutes significant and meaningful change in
health status of individuals and populations. More importantly, the basic
biological and medical criteria that are used for clinical and environmental
judgments require further discussion and clarification. What proportion of loss
of cardio-pulmonary function, overt disability, or mortality is sufficient to
determine an "adverse health effect"? Health-oriented individuals,
including researchers and clinicians, may choose to adhere to different criteria
than other professional groups (e.g., legal, social). It is proposed in this
paper that criteria for defining adverse health effects should represent
clinically meaningful, as distinct from only statistically significant,
responses. These include pulmonary function test results that indicate
obstructive or restrictive diseases, and electrocardiogram results indicating
coronary artery disease. Intraindividual changes that predict a meaningful
medical change would be included; these changes should meet specific
requirements in terms of what constitute normal vs. abnormal ranges of
variation. Further, the proportion of the population defined to be impaired
should be considered. These issues are the focus of this paper.
- Language of Publication
- English
- Unique Identifier
- 88083444
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document
- MeSH Heading (Major)
- Health|*; Health Status|*; Lung Diseases, Obstructive|*DI
- MeSH Heading
- Adult; Blood Pressure Determination; Child; Cholesterol|BL;
Electrocardiography; Human; Models, Biological; Respiratory Function Tests|MT;
Time Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0392-2990
- Country of Publication
- ITALY
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 111 from database: MEDLINE
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- Title
- Community intervention to control plasma lipids.
- Author
- Marmot MG
- Address
- University College London, U.K.
- Source
- Eur Heart J, 1987 Aug, 8 Suppl E:, 71-7
- Abstract
- A necessary part of the strategy of modification of hypercholesterolaemia to
prevent coronary heart disease (CHD) is the detection and treatment, by diet or
by drugs, of high risk individuals. There are several drawbacks to this
approach: (1) the cost of screening to find individuals at risk and of
monitoring by physicians of their therapy; (ii) the problem of labelling
asymptomatic people as 'sick' and advising them on special diets; (iii)
difficulties in compliance. If the community norm is to eat a diet high in fat,
it is difficult for individuals to change, both because it marks them as 'odd'
within the culture and because foods low in saturated fat may be difficult to
obtain and are expensive. A further limitation is that only those individuals at
highest risk may benefit. In a country with a high rate of CHD the problem is
that the mean is high. The aim therefore should be to reduce the population mean
and shift the whole distribution to the left. This suggests a policy of health
education and of policies that remove the barriers against choosing a healthy
diet. Even were such policies to be implemented successfully these alone would
not abolish social and regional differences in CHD mortality.
- Language of Publication
- English
- Unique Identifier
- 88055128
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Community Health Services|*/EC; Coronary Disease|EP/*PC
- MeSH Heading
- Female; Health Education; Human; Male; Smoking|PC
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0195-668X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 112 from database: MEDLINE
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- Title
- Progression of atherosclerosis: the cell biology.
- Author
- Chait A
- Address
- Department of Medicine, University of Washington, Seattle 98195.
- Source
- Eur Heart J, 1987 Aug, 8 Suppl E:, 15-22
- Abstract
- The sequence of events during atherogenesis has been deduced from serial
changes that occur in animal models of atherosclerosis and from autopsy studies
in humans. In vitro studies have provided insight into the mechanisms of the
major features of atherosclerosis. One of the earliest events in atherogenesis
is adhesion of monocytes to intact endothelium, followed by migration along a
chemotactic gradient into the intima, where they become macrophages. These
events appear to be modulated by lipoproteins. Subendothelial macrophages
accumulate cholesteryl ester and become the foam cells of the fatty streak.
Smooth muscle cells proliferate in response to stimulation by mitogens. Later,
intimal macrophages and smooth muscle cells also accumulate lipid, by apparently
different mechanisms. Later, lipoproteins accumulate in the extracellular space
where they are bound to proteoglycans. Strategies to prevent atherosclerosis
should be targeted towards specific events in the cell biology of this disease.
- Language of Publication
- English
- Unique Identifier
- 88055119
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document
- MeSH Heading (Major)
- Arteriosclerosis|*PA; Atherosclerosis|*PA/PP
- MeSH Heading
- Animal; Cholesterol|ME; Endothelium, Vascular|PA; Human; Lipoproteins|PH;
Monocytes|PH; Muscle, Smooth, Vascular|PA; Proteoglycans|ME; Support, U.S.
Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0195-668X
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Lipoproteins); 0 (Proteoglycans); 57-88-5 (Cholesterol)
Record 113 from database: MEDLINE
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- Title
- Individual variation in serum cholesterol levels.
- Author
- Hegsted DM; Nicolosi RJ
- Address
-
- Source
- Proc Natl Acad Sci U S A, 1987 Sep, 84:17, 6259-61
- Abstract
- The intraindividual variances in serum/plasma cholesterol levels from a
variety of sources have been examined. It is apparent that these are very
substantial with mean coefficients of variation usually between 5% and 10%, even
when the diet is controlled in metabolic studies. Some subjects show extreme
variability from one blood sample to the next. Thus, it is very difficult to
assess the degree of risk of individuals according to the guidelines provided by
the Consensus Conference on lowering blood cholesterol levels to prevent heart
disease, and many individuals will be misclassified unless particular attention
is paid to this problem.
- Language of Publication
- English
- Unique Identifier
- 87317632
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document
- MeSH Heading (Major)
- Cholesterol|*BL
- MeSH Heading
- Analysis of Variance; Coronary Disease|ET; Human; Reference Values; Risk;
Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0027-8424
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 114 from database: MEDLINE
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- Title
- Review of lipid-lowering clinical trials in relation to observational
epidemiologic studies.
- Author
- Tyroler HA
- Address
-
- Source
- Circulation, 1987 Sep, 76:3, 515-22
- Abstract
- A review of the experimental clinical trials and observational cohort
evidence relating serum cholesterol level and its reduction to risks of coronary
heart disease (CHD) discloses strong similarities among the quantitative and
qualitative relationships found in these studies. Not only are the risk
functions similar, but the percent reduction observed is the same as that
predicted from the population experience and is proportional to the degree of
cholesterol lowering. Furthermore, the risk function is continuous from the
highest to the lowest serum cholesterol levels studied. These findings confirm
the lipid hypothesis and indicate that lowering serum cholesterol reduces CHD
risk. The understanding and control of CHD requires a dual approach: (1)
identification and treatment of high-risk individuals, and (2) modification of
environmental and behavioral determinants to achieve more favorable
distributions of serum cholesterol in populations.
- Language of Publication
- English
- Unique Identifier
- 87302141
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document
- MeSH Heading (Major)
- Antilipemic Agents|*TU; Cholesterol|*BL; Coronary Disease|EP/*ET;
Hypercholesterolemia|EP/*PC/TH
- MeSH Heading
- Adolescence; Adult; Age Factors; Aged; Cholestyramine|TU; Clinical Trials;
Comparative Study; Diet; Double-Blind Method; Human; Male; Middle Age; Random
Allocation; Risk
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW
- ISSN
- 0009-7322
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antilipemic Agents); 11041-12-6 (Cholestyramine); 57-88-5 (Cholesterol)
Record 115 from database: MEDLINE
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- Title
- Mechanisms and consequences of cellular cholesterol exchange and transfer.
- Author
- Phillips MC; Johnson WJ; Rothblat GH
- Address
-
- Source
- Biochim Biophys Acta, 1987 Jun 24, 906:2, 223-76
- Abstract
- It is apparent from consideration of the reactions involved in cellular
cholesterol homeostasis that passive transfer of unesterified cholesterol
molecules plays a role in cholesterol transport in vivo. Studies in model
systems have established that free cholesterol molecules can transfer between
membranes by diffusion through the intervening aqueous layer. Desorption of free
cholesterol molecules from the donor lipid-water interface is rate-limiting for
the overall transfer process and the rate of this step is influenced by
interactions of free cholesterol molecules with neighboring phospholipid
molecules. The influence of phospholipid unsaturation and sphingomyelin content
on the rate of free cholesterol exchange are known in pure phospholipid bilayers
and similar effects probably occur in cell membranes. The rate of free
cholesterol clearance from cells is determined by the structure of the plasma
membrane. It follows that the physical state of free cholesterol in the plasma
membrane is important for the kinetics of cholesterol clearance and cell
cholesterol homeostasis, as well as the structure of the plasma membrane.
Bidirectional flux of free cholesterol between cells and lipoproteins occurs and
rate constants characteristic of influx and efflux can be measured. The
direction of any net transfer of free cholesterol is determined by the relative
free cholesterol/phospholipid molar ratios of the donor and acceptor particles.
Cholesterol diffuses down its gradient of chemical potential generally
partitioning to the phospholipid-rich particle. Such a surface transfer process
can lead to delivery of cholesterol to cells. This mechanism operates
independently of any lipoprotein internalization by receptor-mediated
endocytosis. The influence of enzymes such as lecithin-cholesterol
acyltransferase and hepatic lipase on the direction of net transfer of free
cholesterol between lipoproteins and cells can be understood in terms of their
effects on the pool sizes and the rate constants for influx and efflux. Excess
accumulation of free cholesterol in cells stimulates the rate of cholesteryl
ester formation and induces deposition of cholesteryl ester inclusions in the
cytoplasm similar to the situation in the 'foam' cells of atherosclerotic
plaque. Clearance of cellular cholesteryl ester requires initial hydrolysis to
free cholesterol followed by efflux of this free cholesterol. The rate of
clearance of cholesteryl ester from cytoplasmic droplets is influenced by the
physical state of the cholesteryl ester; liquid-crystalline cholesteryl ester is
removed more slowly than cholesteryl ester in a liquid state.(ABSTRACT TRUNCATED
AT 400 WORDS)
- Language of Publication
- English
- Unique Identifier
- 87242466
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document
- MeSH Heading (Major)
- Cholesterol|*ME; Membrane Lipids|*PH
- MeSH Heading
- Animal; Biological Transport; Cell Membrane|PH; Cholesterol Esters|ME;
Diffusion; Homeostasis; Human; Membrane Fluidity; Phospholipids|PH; Support,
Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Water
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0006-3002
- Country of Publication
- NETHERLANDS
- CAS Registry/EC Number
- 0 (Cholesterol Esters); 0 (Membrane Lipids); 0 (Phospholipids); 57-88-5
(Cholesterol); 7732-18-5 (Water)
Record 116 from database: MEDLINE
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- Title
- Dietary cholesterol, serum cholesterol, and colon cancer: a review.
- Author
- Broitman SA
- Address
-
- Source
- Adv Exp Med Biol, 1986, 206:, 137-52
- Abstract
- Observational and case-control epidemiologic data supported by experimental
studies indicate that dietary cholesterol may contribute to colon tumorigenesis.
A mechanism for this possible relationship is currently under investigation.
Additional international epidemiologic data, although not uniformly consistent,
indicate an inverse relationship between serum or plasma cholesterol levels and
risk for colon cancer. This risk is greatest at serum cholesterol levels of less
than 180 mg/dl. It has been suggested but not proven that individuals consuming
diets high in dietary fat and cholesterol may have variations in cholesterol
dynamics that account for lowered serum cholesterol levels and enhanced risk for
colon cancer. Clinical evidence in both men and women indicates that
age-sex-adjusted, low serum cholesterol levels may precede the detection of
colon cancer by more than 5 years. Preclinical colon cancer is associated with a
further decrease in serum cholesterol levels. It is not clear whether
progression of the disease before metastatic spread results in continued
lowering of serum cholesterol levels. In men with markedly elevated serum
cholesterol levels who have been placed on cholesterol-lowering drugs such as
clofibrate or cholestyramine, there was no evidence that such regimens increased
the risk for colon cancer. It is possible that reductions in serum cholesterol
associated with the use of these drugs are insufficient to lower cholesterol
levels to a range associated with an increased risk for colon cancer.
- Language of Publication
- English
- Unique Identifier
- 87238012
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Cholesterol, Dietary|*; Colonic Neoplasms|*EP/ET/MO
- MeSH Heading
- Human; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0065-2598
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol, Dietary); 57-88-5 (Cholesterol)
Record 117 from database: MEDLINE
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- Title
- Interstitial fluid lipoproteins.
- Author
- Sloop CH; Dory L; Roheim PS
- Address
-
- Source
- J Lipid Res, 1987 Mar, 28:3, 225-37
- Abstract
- While a wide variety of techniques has been used to collect samples of
interstitial fluid, most of our detailed knowledge about the composition of
interstitial fluid lipoproteins has come from lymph collection studies. The
considerable variability of lymph data probably reflects the effect of variable
metabolic modification and different capillary permeabilities on the lipoprotein
composition of interstitial fluid. All density classes of plasma lipoproteins
are present in lymph. In peripheral lymph, the lymph/plasma concentration ratios
of lipoproteins vary from 0.03 for VLDL-sized particles to 0.2 for HDL. Lymph
from more permeable vascular beds, such as lung and myocardium, contains
proportionately more lipoproteins. Their lymph/plasma concentration ratios vary
from 0.1 to 0.6. In general, lymph lipoproteins are more heterogeneous in size
than their plasma counterparts. Lymph HDL and LDL contain larger and smaller
particles than their plasma equivalents. Lymph lipoproteins have unusual shapes
(square packing and discoidal), chemical compositions, and molecular charge,
which suggest de novo formation and/or extensive peripheral modification. Lymph
HDL and LDL are enriched in free cholesterol. Lymph HDL also has increased
cholesterol/protein and phospholipid/protein (especially sphingomyelin) ratios
(Sloop, C.H., L. Dory, and P.S. Roheim, unpublished observations). Lymph HDL
apoprotein composition differs from that of plasma, with an increase in apoE and
apoA-IV content relative to apoA-I. These discoidal HDL particles may be
products of an initial stage of reverse cholesterol transport. We believe
further study of their metabolic fate would give important information
concerning the later stages of reverse cholesterol transport.
- Language of Publication
- English
- Unique Identifier
- 87196972
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document
- MeSH Heading (Major)
- Extracellular Space|*ME; Lipoproteins|*ME
- MeSH Heading
- Animal; Cholesterol|ME; Human; Lipoproteins, HDL|ME; Lipoproteins, LDL|ME;
Lymph|ME; Support, U.S. Gov't, P.H.S.; Tissue Distribution
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0022-2275
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 0 (Lipoproteins, HDL); 57-88-5 (Cholesterol)
Record 118 from database: MEDLINE
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- Title
- Mode of hypocholesterolemic action of probucol in animals and man.
- Author
- Beynen AC
- Address
-
- Source
- Artery, 1987, 14:2, 113-26
- Abstract
- Probucol is a widely used serum-cholesterol lowering drug. It is proposed
that in humans probucol stimulates the plasma clearance of low density
lipoproteins (LDL), which accounts for the drug-induced decrease in LDL
cholesterol levels. In the liver the enhanced uptake of LDL cholesterol
stimulates the conversion of cholesterol into bile acids, which in turn causes
an increase in the output of bile acids with the feces. The increased flux
through the bile acid biosynthesis pathway tends to deplete the liver pools of
cholesterol. This causes stimulation of cholesterol synthesis, which is
associated with a higher hepatic efflux of LDL. Thus in humans taking probucol
cholesterol turnover is enhanced. In this way a new equilibrium is reached in
which LDL production equals LDL catabolism, and in which cholesterol turnover is
increased. The probucol-induced reduction in high density lipoprotein (HDL)
cholesterol may be caused by inhibition of HDL synthesis. If we assume that the
absolute rate of HDL clearance from the plasma is proportional to HDL
concentration, then serum HDL will settle at a new, lower level where the
clearance rate equals the rate of production. In contrast to humans, probucol
may decrease the turnover of cholesterol in rats. The relatively large amounts
of probucol generally fed inhibit cholesterol absorption, and this may account
for the reduction in serum total cholesterol, which essentially represents HDL
cholesterol. The decrease in absorption diminishes intestinal formation of HDL,
which in turn leads to a diminished flux of serum cholesterol into the liver,
and causes inhibition of bile acid synthesis because substrate availability is
depressed. The effect of probucol on cholesterol synthesis is not clear, but the
drug must lower the sum of cholesterol absorption and synthesis. In this way,
serum cholesterol settles at a new, lower level, where cholesterol input equals
its output.
- Language of Publication
- English
- Unique Identifier
- 87184018
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document
- MeSH Heading (Major)
- Hypercholesterolemia|BL/*DT; Phenols|*TU; Probucol|*TU
- MeSH Heading
- Animal; Cholesterol|BL/ME; Human; Lipoproteins, HDL Cholesterol|BL;
Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL|ME; Rats; Species
Specificity
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0098-6127
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL Cholesterol); 0
(Lipoproteins, VLDL Cholesterol); 0 (Lipoproteins, VLDL); 0 (Phenols);
23288-49-5 (Probucol); 57-88-5 (Cholesterol)
Record 119 from database: MEDLINE
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- Title
- Synovial fluid lipid abnormalities in various disease states: review and
classification.
- Author
- Wise CM; White RE; Agudelo CA
- Address
-
- Source
- Semin Arthritis Rheum, 1987 Feb, 16:3, 222-30
- Abstract
- Although lipids are not usually present in large quantities in normal
synovial fluids or in the usual synovial fluid seen in most rheumatologic
conditions, their presence in synovial fluid may have diagnostic importance. As
summarized in Table 2, analysis of synovial fluids for lipid constituents is
relatively simple. On standing or after centrifugation, significant amounts of
lipids may layer out and be visible as a supernatant. On microscopic
examination, lipid droplets are usually easily seen and should be stainable with
appropriate dyes (oil red O or Sudan III or IV), or may occasionally be
visualized as intracellular or extracellular inclusions by polarized microscopy.
Small (0.5 to 2.0 microns) intracellular inclusions containing triglycerides may
be seen in neutrophils from most synovial fluids, and are of no diagnostic
importance. Cholesterol crystals may be readily recognized microscopically by
their characteristic flat, plate-like appearance and notched corners Synovial
fluid may also be analyzed for cholesterol and triglycerides in routine clinical
laboratories, and free fatty acids and lipolytic enzymes in special lipid
laboratories. The presence of massive increases in cholesterol associated with
microscopically visible cholesterol crystals is usually associated with chronic
RA, occasionally in the setting of super-imposed bacterial infection. The
presence of gross or microscopic lipid droplets is usually associated with
trauma and hemorrhagic effusions. When present in this setting, the clinician
should entertain a high suspicion for a significant intraarticular injury, such
as fracture, meniscal tear, or severe ligamentous injury. In addition, however,
several instances of non-traumatic inflammatory effusions associated with
intracellular and extracellular lipid droplets have been reported.(ABSTRACT
TRUNCATED AT 250 WORDS)
- Language of Publication
- English
- Unique Identifier
- 87149114
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document
- MeSH Heading (Major)
- Joint Diseases|*ME; Lipids|*ME; Synovial Fluid|*ME
- MeSH Heading
- Cholesterol|ME; Chyle|ME; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0049-0172
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 120 from database: MEDLINE
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- Title
- Cholesterol metabolism and aging.
- Author
- Kreisberg RA; Kasim S
- Address
-
- Source
- Am J Med, 1987 Jan 26, 82:1B, 54-60
- Abstract
- Changes occur in lipid and lipoprotein concentrations with age that increase
the risk of developing atherosclerotic disease. In children and young adults
(less than 20 years of age), the plasma total cholesterol concentration
decreases between the ages of 10 and 20 years. After age 20, the plasma total
cholesterol concentration increases progressively, and in men reaches a plateau
between the ages of 50 and 60 years, whereas in women, it reaches a peak between
60 and 70 years of age. The low-density lipoprotein cholesterol concentration
increases progressively in men and women after age 20, but more rapidly in men,
accounting for most of the overall gender difference in total cholesterol. The
rate at which the low-density lipoprotein cholesterol concentration increases in
women begins to accelerate between 40 and 50 years of age, and the concentration
exceeds that in men by 55 to 60 years. High-density lipoprotein cholesterol
concentrations decrease in males during puberty and early adulthood, and
thereafter remain lower than those in women at all comparable ages. The
high-density lipoprotein cholesterol concentrations remain constant in women
throughout their lifetime. Beyond 30 years of age, women taking estrogen
preparations have higher high-density lipoprotein cholesterol concentrations
than women who are not taking estrogens. The triglyceride concentration
increases progressively in men, reaching peak values between 40 and 50 years of
age, and then declining slightly thereafter. In women, the triglyceride
concentration increases throughout their lifetime, but is always higher in those
using estrogens. Whether these changes in lipoprotein concentrations merely
accompany the increasing prevalence of atherosclerotic vascular disease that
occurs with age, or contribute to it, is unknown at this time.
- Language of Publication
- English
- Unique Identifier
- 87124882
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document
- MeSH Heading (Major)
- Aging|*ME; Cholesterol|*ME; Coronary Disease|*ME
- MeSH Heading
- Adult; Aged; Female; Human; Lipoproteins, HDL Cholesterol|ME; Lipoproteins,
LDL Cholesterol|ME; Male; Middle Age; Triglycerides|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9343
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL Cholesterol); 0
(Triglycerides); 57-88-5 (Cholesterol)
Record 121 from database: MEDLINE
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- Title
- Regulation of plasma cholesterol by hepatic low-density lipoprotein
receptors.
- Author
- Kovanen PT
- Address
-
- Source
- Am Heart J, 1987 Feb, 113:2 Pt 2, 464-9
- Abstract
- The endogenous lipoprotein system (very low-density lipoprotein [VLDL],
intermediate-density lipoprotein [IDL], low-density lipoprotein [LDL] cascade)
holds the key to understanding the mechanisms by which hormones, diet, and drugs
interact to regulate the plasma cholesterol level. Crucial components of this
system are hepatic LDL receptors that mediate the uptake and degradation of
plasma LDL. With experimental animals, it has been possible to demonstrate that
hepatic LDL receptors are sensitive to hormonal, dietary, and pharmacologic
manipulation. The decrease in number of hepatic LDL receptors in hypothyroidism
or after cholesterol feeding leads to elevation of plasma LDL cholesterol
levels. Conversely, the increase in number of hepatic LDL receptors results in
lowering of plasma LDL cholesterol levels. This can be observed in
hyperthyroidism, during administration of pharmacologic doses of 17
alpha-ethinyl estradiol, or during treatment with cholesterol-lowering drugs
such as the bile acid-binding resins and cholesterol-synthesis inhibitors. Since
cholesterol excretion from the body occurs via the liver, the increased
efficiency of disposal of plasma cholesterol by increasing hepatic LDL receptors
will ultimately lead to depletion of excessive body cholesterol. Pharmacologic
regulation of hepatic LDL receptors should be a valuable tool in the prevention
and therapy of atherosclerosis.
- Language of Publication
- English
- Unique Identifier
- 87124368
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Liver|*PH; Receptors, LDL|*PH
- MeSH Heading
- Animal; Cholesterol, Dietary|AD; Disease Models, Animal; Dogs; Human;
Hypercholesterolemia, Familial|BL; Lipoproteins, LDL Cholesterol|BL; Rabbits;
Rats
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-8703
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol, Dietary); 0 (Lipoproteins, LDL Cholesterol); 0 (Receptors,
LDL); 57-88-5 (Cholesterol)
Record 122 from database: MEDLINE
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- Title
- The promise of enzymes in therapy of hyperlipidemia.
- Author
- Setälä K
- Address
-
- Source
- Med Hypotheses, 1986 Jul, 20:3, 287-315
- Abstract
- Treatment of hyperlipidemias must be commenced in that intestinal segment
where alimentary lipoprotein aggregate generation is initiated postprandially
and the aggregates are still in nascent form. This is to prevent the formation
of potentially pathological units that do not equilibrate with the blood
colloid. The colloid chemical state of the alimentary lipoprotein entities in
the systemic circulation is decisive for maintenance of their stability and for
their disposal from the blood. The causes of impaired, "unripe,"
lipoprotein aggregate formation include: (a) the action of human pancreatic
lipase is even normally a restricted and vulnerable process, (b) inadequate
ratio of protein to fat to stabilize the aggregates, (c) defective proteolysis
in the small intestine, and (d) the dual behavior of the surface
tension-lowering agent, the lecithin antagonist cholesterol. On the one hand,
cholesterol represents physicochemically the weakest link in the lipoprotein
interfaces. On the other hand, an excess of cholesterol in lipoprotein
interfaces decreases the stability of the surface film. This leads to changes in
the decay of the entities and the cell surface-active lipid constituents of the
"unripe" plasma lipoprotein colloid complexes can easily be adsorbed
to the endothelial cell surface plasma membrane: the excess
aggregate-cholesterol molecules simply join, or dissolve in, the cell
membrane-cholesterol which thus acts as its own receptor or solvent: cholesterol
dimers occur. This causes rigidity of the endothelial cell surface membrane and
leads to impaired cell metabolism. The intima recognizes the impairment as a
foreign body and initiates a physiological defense reaction including
phagocytosis. The event may be still more dangerous if the adrenergic receptors
of the autonomous nervous system involved in lipolysis with subsequent plasma
efflux are simultaneously stimulated. The therapeutic measure indicated is
production of balanced alimentary lipoprotein aggregates. This can be achieved
by oral administration of (a) protease, and (b) non-specific micellar lipase.
The lipase functions without restriction and can perform all the activities that
human pancreatic lipase cannot. The enzymes utilized are of mold origin and
generally available.
- Language of Publication
- English
- Unique Identifier
- 86310421
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document
- MeSH Heading (Major)
- Hyperlipidemia|*DT; Lipase|*TU; Peptide Hydrolases|*TU
- MeSH Heading
- Adipose Tissue|ME; Animal; Atherosclerosis|ET; Chemoreceptors|PH;
Cholesterol|PH; Chylomicrons|BL/RE; Clinical Trials; Histamine|PD; Human;
Lipoproteins|ME; Mice; Proteins|BI; Receptors, Adrenergic|PH
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW
- ISSN
- 0306-9877
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- EC 3.1.1.3 (Lipase); EC 3.4 (Peptide Hydrolases); 0 (Chylomicrons); 0
(Lipoproteins); 0 (Receptors, Adrenergic); 51-45-6 (Histamine); 57-88-5
(Cholesterol)
Record 123 from database: MEDLINE
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- Title
- Effect of ursodeoxycholic acid and chenodeoxycholic acid on cholesterol and
bile acid metabolism.
- Author
- Tint GS; Salen G; Shefer S
- Address
-
- Source
- Gastroenterology, 1986 Oct, 91:4, 1007-18
- Abstract
- Orally administered UDCA dramatically reduces the secretion of cholesterol
into the bile. During UDCA therapy cholesterol balance is maintained by a
reduction in both the relative and absolute absorption of cholesterol and,
perhaps, by a combined moderate enhancement of bile acid synthesis and a
suppression of cholesterol production. The percentage of UDCA in the bile is
limited by the inability of UDCA to suppress bile acid synthesis from
cholesterol and by the conversion of UDCA to CDCA by the intestinal bacteria.
- Language of Publication
- English
- Unique Identifier
- 86301701
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document
- MeSH Heading (Major)
- Bile Acids and Salts|*ME; Chenodeoxycholic Acid|PD/*TU;
Cholelithiasis|*DT/ME; Cholesterol|*ME; Deoxycholic Acid|*AA; Ursodeoxycholic
Acid|PD/*TU
- MeSH Heading
- Animal; Human; Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.;
Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0016-5085
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 128-13-2 (Ursodeoxycholic Acid); 474-25-9
(Chenodeoxycholic Acid); 57-88-5 (Cholesterol); 83-44-3 (Deoxycholic Acid)
Record 124 from database: MEDLINE
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- Title
- Serum-cholesterol response to dietary cholesterol: a re-evaluation.
- Author
- Hegsted DM
- Address
-
- Source
- Am J Clin Nutr, 1986 Aug, 44:2, 299-305
- Abstract
- The data from the literature in which the serum-cholesterol response has
been measured following a change in cholesterol intake have been re-evaluated.
The overall data appear to be best explained by exponential equations. However,
very large differences in response have been reported for similar changes in
cholesterol intake and no predictive equation can explain such values. It is
concluded that over the range of cholesterol intakes of practical interest--0 to
400 mg/1000 kcal--the usual response is approximately linear, each 1 mg/1000
kcal resulting in an expected increase of serum cholesterol of approximately 0.1
mg/dl. With a 2500 kcal diet, an increase in intake of 100 mg/day would be
expected to increase serum cholesterol by approximately 4 mg/dl.
- Language of Publication
- English
- Unique Identifier
- 86265431
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Cholesterol, Dietary|*ME
- MeSH Heading
- Human; Regression Analysis; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9165
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol, Dietary); 57-88-5 (Cholesterol)
Record 125 from database: MEDLINE
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- Title
- Formation and transport of chylomicrons by enterocytes to the lymphatics.
- Author
- Tso P; Balint JA
- Address
-
- Source
- Am J Physiol, 1986 Jun, 250:6 Pt 1, G715-26
- Abstract
- Digestion of triglyceride in the intestine results in the production of
2-monoglyceride and fatty acid. Phosphatidylcholine is hydrolyzed in the lumen
to form lysophosphatidylcholine before its absorption. These digestion products
are absorbed by the enterocytes through simple diffusion. In contrast,
cholesterol absorption seems specific and is energy dependent. After entry into
the enterocytes, these lipid digestion products migrate to the endoplasmic
reticulum. Both fatty acid-binding protein and sterol carrier protein may be
involved in the intracellular transport of fatty acid and cholesterol,
respectively. Through predominantly the monoglyceride pathway, monoglycerides
and fatty acids are resynthesized to form triglyceride in the endoplasmic
reticulum. The lipid droplets, coated with cholesterol, phospholipid, and
apolipoproteins, are then further processed in the Golgi apparatus before being
released by the enterocytes through exocytosis. As yet, little is known of the
factors regulating the formation and release of these chylomicrons by the
enterocytes. Although apolipoprotein B is a prerequisite for the formation of
chylomicrons, the question of whether its supply is rate limiting for
chylomicron formation remains to be demonstrated. Other factors that may play a
role in chylomicron formation are luminal phospholipid supply, Ca2+, and
microtubules. Chylomicrons and very low-density lipoproteins are probably
produced by the enterocytes via different pathways. For example, Pluronic L-81,
a hydrophobic surfactant, affects only chylomicron formation and has little
effect on very low-density lipoprotein production. The movement of chylomicrons
from the intercellular space through the basement membrane to the lamina propria
is not fully understood. Once inside the lamina propria, the movement of
chylomicrons is probably by diffusion and is greatly facilitated by interstitial
hydration; thus the lymphogogic effect of fat absorption may serve an important
function for the transfer of chylomicrons from the enterocytes to the lacteal.
- Language of Publication
- English
- Unique Identifier
- 86239622
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document
- MeSH Heading (Major)
- Chylomicrons|*ME; Intestine, Small|*ME/UL; Lymphatic System|*ME
- MeSH Heading
- Animal; Basement Membrane|ME; Biological Transport; Carrier Proteins|ME;
Cholesterol|ME; Endoplasmic Reticulum|ME; Exocytosis; Fatty Acids|ME; Golgi
Apparatus|ME; Human; Intestinal Absorption; Lipids|ME; Lipoproteins|ME;
Lipoproteins, VLDL|ME; Microscopy, Electron; Phospholipids|ME; Support, U.S.
Gov't, P.H.S.; Triglycerides|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9513
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (non-specific lipid transfer protein); 0 (sterol carrier protein(1)); 0
(Carrier Proteins); 0 (Chylomicrons); 0 (Fatty Acids); 0 (Lipoproteins); 0
(Lipoproteins, VLDL); 0 (Phospholipids); 0 (Triglycerides); 57-88-5
(Cholesterol)
Record 126 from database: MEDLINE
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- Title
- Role of risk factor management in progression and regression of coronary and
femoral artery atherosclerosis.
- Author
- Glueck CJ
- Address
-
- Source
- Am J Cardiol, 1986 May 30, 57:14, 35G-41G
- Abstract
- The results of 3 recently completed studies usher in a new era in the
treatment of coronary atherosclerosis and its sequelae. In aggregate, these
results show that reductions in low density lipoprotein (LDL) cholesterol or
reductions in the ratio of total to high density lipoprotein (HDL) cholesterol
by either diet or drugs or both are effective in primary and secondary
prevention of coronary artery disease (CAD). In the Lipid Research Clinics'
Coronary Primary Prevention Trial, reducing levels of LDL cholesterol,
regardless of whether the primary intervention was diet or drug, correlated with
a reduction in CAD events. In the National Heart, Lung, and Blood Institute's
Type II Coronary Intervention Study, CAD progression at 5 years was inversely
related to a change in the ratio of HDL cholesterol to total cholesterol. In the
Leiden Intervention Trial, cessation of coronary artery atherosclerotic lesion
growth correlated with the ratio of total cholesterol to HDL cholesterol.
Several trials now under way will test the effects of much more substantial
reductions of LDL cholesterol (up to 50%) and increments in HDL cholesterol (up
to 25%) on interrupting the progression or inducing the regression of coronary
artery atherosclerosis. Even small reductions in the progression of coronary
artery lesions or induction of their regression should produce major reductions
in morbidity and mortality from CAD. The importance of secondary prevention also
extends to patients after coronary artery bypass surgery, because the likelihood
of graft occlusion is likewise related to the patient's lipid profile. Further,
the importance of primary prevention of atherosclerosis through modification of
lipids and lipoprotein cholesterol in the first-degree relatives of young
victims of atherosclerosis cannot be overemphasized.
- Language of Publication
- English
- Unique Identifier
- 86239023
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document
- MeSH Heading (Major)
- Arteriosclerosis|*TH; Atherosclerosis|CO/*TH; Coronary Disease|ET/PC/*TH;
Femoral Artery|*
- MeSH Heading
- Cholesterol|BL; Cholesterol, Dietary|AD; Coronary Artery Bypass; Female;
Human; Hyperlipidemia|TH; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL
Cholesterol|BL; Male; Primary Prevention; Risk; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol, Dietary); 0 (Lipoproteins, HDL Cholesterol); 0
(Lipoproteins, LDL Cholesterol); 57-88-5 (Cholesterol)
Record 127 from database: MEDLINE
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- Title
- Partial ileal bypass surgery in the treatment of heterozygous familial
hypercholesterolemia: a review.
- Author
- Schouten JA; Beynen AC
- Address
-
- Source
- Artery, 1986, 13:4, 240-63
- Abstract
- Partial ileal bypass (PIB) surgery is a method in the treatment of
heterozygous familial hypercholesterolemia (FH). Since the first report in 1964
about 150 cases of FH who underwent the surgical procedure have been described.
This number is very low when compared to other types of cholesterol-lowering
treatment. On average, PIB decreases the level of plasma total cholesterol by
35% in FH patients, and the surgical procedure can be considered the most
effective, single cholesterol-lowering method. PIB-induced reduction of plasma
cholesterol is permanent. Further decrease of plasma cholesterol may be obtained
in combination with an inhibitor of cholesterol biosynthesis. PIB specifically
lowers plasma LDL cholesterol; the concentration of HDL cholesterol is not
systematically influenced. The mechanism underlying the hypocholesterolemic
action of PIB is discussed. Until now there is no evidence that PIB reduces
atherosclerotic coronary death in FH patients. After PIB more patients
experience improvement of angina pectoris rather than deterioration (15 versus 2
out of 41), but the number of patients is too small to allow solid conclusions.
In 50% of FH patients PIB may cause regression of xanthomata. Out of 209
hyperlipidemic patients described, 14 patients had postoperative complications,
which caused death in 3 patients. Diarrhea is the most common side-effect of
PIB; out of 99 operated patients serious diarrhea troubled 38 patients, whereas
40 patients had minor complaints during the first year postoperatively. Diarrhea
may persist as long as 10 years after PIB. There is no evidence that PIB
enhances gallstone formation and severely impairs liver function, but PIB may
increase the incidence of renal stones. It is suggested that PIB can be
considered in the treatment of FH. However, in each individual case the
disadvantages and possible advantages should be carefully weighed out, and this
consideration should form the basis to decide whether or not surgery is
indicated.
- Language of Publication
- English
- Unique Identifier
- 86214578
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document
- MeSH Heading (Major)
- Hypercholesterolemia, Familial|GE/*TH; Jejunoileal Bypass|*; Postoperative
Complications|*ET
- MeSH Heading
- Bile Acids and Salts|ME; Body Weight; Cholelithiasis|ET; Cholesterol|BL;
Coronary Disease|PC; Diarrhea|ET; Heterozygote; Human; Intestinal Absorption;
Kidney Calculi|ET; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL
Cholesterol|BL; Liver Function Tests; Xanthomatosis|PC
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0098-6127
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 0 (Lipoproteins, HDL Cholesterol); 0
(Lipoproteins, LDL Cholesterol); 57-88-5 (Cholesterol)
Record 128 from database: MEDLINE
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- Title
- Medical management of cholesterol gallstones.
- Author
- Abate MA
- Address
-
- Source
- Drug Intell Clin Pharm, 1986 Feb, 20:2, 106-15
- Abstract
- Cholesterol gallstones are a significant cause of morbidity in the U.S.
Methods used to treat gallstones include cholecystectomy or medical dissolution.
The primary drugs used for the dissolution of cholesterol gallstones are two
bile acids, chenodeoxycholic acid and ursodeoxycholic acid. Complete or partial
gallstone dissolution rates using chenodeoxycholic acid have ranged from 30 to
80 percent. Factors affecting gallstone dissolution using the bile acids include
the dosage and administration schedule, obesity, the stone characteristics,
diet, and the duration of therapy. The adverse effects of chenodeoxycholic acid
include gastrointestinal complaints, hepatotoxicity, and increased serum
cholesterol. Ursodeoxycholic acid, which is investigational, differs from
chenodeoxycholic acid in its mechanism of action. Ursodeoxycholic acid has
similar efficacy with chenodeoxycholic acid, at a lower daily dosage, with less
gastrointestinal and hepatic adverse effects. If appropriate patient selection
is used, the response rate to medical therapy can range from 50 to 80 percent.
- Language of Publication
- English
- Unique Identifier
- 86135454
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document
- MeSH Heading (Major)
- Cholelithiasis|*DT/ME/SU; Cholesterol|*ME
- MeSH Heading
- Bile|ME; Chenodeoxycholic Acid|AD/AE/TU; Cholecystectomy; Human;
Ursodeoxycholic Acid|AD/AE/TU
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0012-6578
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 128-13-2 (Ursodeoxycholic Acid); 474-25-9 (Chenodeoxycholic Acid); 57-88-5
(Cholesterol)
Record 129 from database: MEDLINE
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- Title
- Atherosclerosis and lipoprotein metabolism: role of reverse cholesterol
transport.
- Author
- Roheim PS
- Address
-
- Source
- Am J Cardiol, 1986 Feb 12, 57:5, 3C-10C
- Abstract
- To understand the complexity of lipoprotein metabolism and its influence on
atherosclerosis, one must be aware of the physiologic characteristics and
functions of the different lipoprotein classes, apolipoproteins and enzymes.
Understanding of the dynamics of cholesterol and lipoprotein metabolism,
especially reverse cholesterol transport, will aid in finding a means of
preventing and reversing the atherosclerotic process.
- Language of Publication
- English
- Unique Identifier
- 86127058
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document
- MeSH Heading (Major)
- Arteriosclerosis|*ET; Atherosclerosis|*ET; Cholesterol|*ME; Lipoproteins|*ME
- MeSH Heading
- Apolipoproteins|AN/PH; Biological Transport; Chylomicrons|AN; Extracellular
Space|ME; Human; Lecithin Acyltransferase|AN; Lipoprotein Lipase|PH;
Lipoproteins, HDL|ME; Lipoproteins, LDL|ME; Lipoproteins, VLDL|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 2.3.1.43 (Lecithin Acyltransferase); EC 3.1.1.34 (Lipoprotein Lipase); 0
(Apolipoproteins); 0 (Chylomicrons); 0 (Lipoproteins); 0 (Lipoproteins, HDL); 0
(Lipoproteins, VLDL); 57-88-5 (Cholesterol)
Record 130 from database: MEDLINE
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- Title
- An approach to the management of hyperlipoproteinemia.
- Author
- Hoeg JM; Gregg RE; Brewer HB Jr
- Address
-
- Source
- JAMA, 1986 Jan 24-31, 255:4, 512-21
- Abstract
- Recent clinical trials indicate that reduction of plasma cholesterol
concentrations in individuals with increased levels of low-density lipoproteins
reduces their risk of myocardial infarction and death. Therefore, the question
of "whether to treat" should be shifted to "whom to treat"
and "how best to treat". The understanding of normal lipid transport
via the plasma lipoproteins has grown to a sophisticated level over the past 20
years. Plasma cholesterol, required for cellular membrane integrity, and plasma
triglycerides, the primary mammalian energy source, are carried in lipoprotein
particles that vary in size, density, lipid composition, and apolipoprotein
content. Some lipoprotein particles (low-density lipoproteins) play a causal
role in the atherosclerotic process, while other particles (high-density
lipoproteins) appear to prevent this process. Utilizing this understanding of
the plasma lipoproteins, a systematic approach to the management of the patient
with hyperlipoproteinemia has been developed which may lead to the normalization
of plasma lipoprotein concentrations in the majority of hyperlipoproteinemic
patients.
- Language of Publication
- English
- Unique Identifier
- 86089520
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document
- MeSH Heading (Major)
- Hyperlipoproteinemia|BL/DI/*TH
- MeSH Heading
- Anticholesteremic Agents|TU; Cholesterol|BL; Human; Hypercholesterolemia|DT;
Hyperlipidemia|TH; Lipids|ME; Lipoproteins|ME; Lipoproteins, HDL Cholesterol|BL;
Lipoproteins, LDL Cholesterol|BL; Lipoproteins, VLDL|BL; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0098-7484
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Anticholesteremic Agents); 0 (Lipoproteins); 0 (Lipoproteins, HDL
Cholesterol); 0 (Lipoproteins, LDL Cholesterol); 0 (Lipoproteins, VLDL
Cholesterol); 0 (Lipoproteins, VLDL); 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 131 from database: MEDLINE
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- Title
- Stress, personality and serum-cholesterol level.
- Author
- van Doornen LJ; Orlebeke KF
- Address
-
- Source
- J Human Stress, 1982 Dec, 8:4, 24-9
- Abstract
- It appears that serum-cholesterol level may serve as an important mediator
between psychological variables and coronary heart disease (CHD). From a review
of the literature it is concluded that (1) psychological stressors significantly
elevate serum-cholesterol level and (2) psychological characteristics like the
Type A-pattern and depression are positively correlated with serum-cholesterol
levels. This suggests that the relationship between CHD and stress and coronary
prone behavior may be partially explained by the mediating role of
serum-cholesterol. A more careful consideration of psychological variables may
be helpful in reducing the substantial amount of unexplained variance in
cholesterol levels.
- Language of Publication
- English
- Unique Identifier
- 83162265
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Personality|*; Stress, Psychological|*BL
- MeSH Heading
- Adult; Coronary Disease|BL/PX; Emotions; Female; Human; Male; Middle Age;
Risk; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0097-840X
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 132 from database: MEDLINE
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- Title
- High-density lipoprotein cholesterol: methods and clinical significance.
- Author
- Durrington PN
- Address
-
- Source
- Crit Rev Clin Lab Sci, 1982, 18:1, 31-78
- Abstract
- The known limitations and advantages of methods for determining serum
high-density lipoprotein (HDL) cholesterol concentration are reviewed with
special emphasis on the applicability of each method to clinical medicine. The
evidence for and against the relevance of serum HDL cholesterol to the
prediction of the likelihood of an individual man or woman developing clinically
evident ischemic heart disease is discussed. The possibility that HDL
subfractions may be more relevant to this issue is also discussed. Information
about serum HDL cholesterol concentration in diseases other than ischemic heart
disease is reviewed. The effect of diet, body-weight, exercise,
cigarette-smoking, alcohol intake, and hyperlipoproteinemia and the effect of
modification of these factors on serum HDL cholesterol levels is discussed.
Finally, a practical approach to the patient with a low concentration of serum
HDL cholesterol is suggested.
- Language of Publication
- English
- Unique Identifier
- 83104125
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document
- MeSH Heading (Major)
- Cholesterol|*BL/ME; Lipoproteins, HDL|*BL/IP/ME/PH
- MeSH Heading
- Alcohol, Ethyl|PD; Antilipemic Agents|PD; Chemistry; Cholesterol Esters|ME;
Diabetes Mellitus|BL; Dietary Carbohydrates|PD; Dietary Fats|PD; Exertion;
Human; Hyperlipidemia|BL; Lipolysis; Obesity|ME; Thyroid Diseases|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 1040-8363
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antilipemic Agents); 0 (Cholesterol Esters); 0 (Dietary Fats); 0
(Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL); 57-88-5 (Cholesterol);
64-17-5 (Alcohol, Ethyl)
Record 133 from database: MEDLINE
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- Title
- The hepatobiliary axis and lipoprotein metabolism: effects of bile acid
sequestrants and ileal bypass surgery.
- Author
- Packard CJ; Shepherd J
- Address
-
- Source
- J Lipid Res, 1982 Nov, 23:8, 1081-98
- Abstract
- Cholesterol excretion from the body is achieved almost exclusively via the
hepatobiliary axis. Disruption of the integrity of this pathway by interruption
of the enterohepatic circulation produces profound changes in cholesterol
metabolism that affect every body tissue. This is particularly evident in the
liver and gut which are the major sources of this sterol in the plasma. Elevated
plasma cholesterol levels have been implicated in the pathogenesis of
atherosclerosis and, in consequence, strenuous efforts have been made to find
appropriate hypocholesterolemic therapy to reduce this risk. Medical or surgical
interruption of the enterohepatic circulation is, to date, the most successful
means of lowering plasma cholesterol, and in this review we examine the
ramifications of such therapy on lipid and lipoprotein metabolism in the liver,
gut, and plasma.
- Language of Publication
- English
- Unique Identifier
- 83084423
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document
- MeSH Heading (Major)
- Bile|*ME; Bile Acids and Salts|*ME; Ileum|*SU; Lipoproteins|BL/*ME;
Liver|*ME
- MeSH Heading
- Animal; Cholesterol|ME; Enterohepatic Circulation; Human; Intestines|ME;
Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0022-2275
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 0 (Lipoproteins); 57-88-5 (Cholesterol)
Record 134 from database: MEDLINE
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- Title
- Reduction of low density and high density lipoprotein cholesterol by
fat-modified diets. A survey of recent findings.
- Author
- Vessby B; Lithell H; Boberg J
- Address
-
- Source
- Hum Nutr Clin Nutr, 1982, 36:3, 203-11
- Abstract
- The aim of this review is to summarize recent findings concerning the
effects of fat-modified diets on serum lipoproteins, especially on high density
lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol concentrations.
Generally, both HDL and LD cholesterol are reduced in subjects on diets enriched
in polyunsaturated fatty acids (PUFA diets). The only exceptions to this rule
are hypertriglyceridaemic patients with low HDL or LDL concentrations. The
changes in HDL and LDL cholesterol are inversely related to the respective HDL
and LDL concentrations before dietary treatment. Increasing HDL cholesterol
concentrations are seen only during simultaneous body weight reduction. Low HDL
cholesterol concentrations are not normalized on PUFA diets. The ratio of LDL
cholesterol to HDL cholesterol shows only marginal changes during treatment with
a PUFA diet. Thus we cannot clearly state how a lipid-lowering diet might
contribute to the anti-atherogenic effect which seems to be characteristic of
this type of diet, on the basis not of the change in fasting serum lipoprotein
concentrations, but of epidemiological and experimental data.
- Language of Publication
- English
- Unique Identifier
- 83006559
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Dietary Fats|*PD/TU; Hyperlipoproteinemia|*BL;
Lipoproteins, HDL|*BL; Lipoproteins, LDL|*BL
- MeSH Heading
- Adolescence; Adult; Aged; Atherosclerosis|PC; Coronary Disease|PC; Diet;
Fats, Unsaturated|PD/TU; Fatty Acids, Unsaturated|PD; Female; Human;
Lipoproteins|BL; Male; Middle Age; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Dietary Fats); 0 (Fats, Unsaturated); 0 (Fatty Acids, Unsaturated); 0
(Lipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL); 0
(Lipoproteins, LDL Cholesterol); 57-88-5 (Cholesterol)
Record 135 from database: MEDLINE
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- Title
- Diet and coronary heart disease.
- Author
- Stamler J
- Address
-
- Source
- Biometrics, 1982 Mar, 38 Suppl:, 95-118
- Abstract
- This paper reviews key aspects of the relationship of diet to coronary heart
disease, as demonstrated in epidemiologic and other research over the last 25 or
more years. It summarizes the extensive findings that have demonstrated an
etiologically significant association among dietary lipid, serum cholesterol,
and coronary heart disease; between caloric imbalance and two of the major CHD
risk factors, hypertension and hypercholesterolemia; on the relationship between
habitual diet high in sodium and hypertension. It also reviews the data on the
relationship of habitual dietary lipid intake of individuals within a population
to the serum cholesterol and CHD risk of individuals, indicating that valid
positive findings in this area are consistent with evidence from
cross-population epidemiologic studies, controlled experiments on diet change in
man, and findings from animal research. It delineates the controlled experiments
on diet change in man, and findings from animal research. It delineates the
methodological problems that have stood in the way of the sound elucidation of
this matter, and of the similar ones making it difficult to fully resolve the
issue of the relationship of habitual dietary sodium intake of individuals
within a population to their blood pressure. It reviews recent findings on the
relationship of diet, particularly dietary lipid and calorie balance, to
fractions of plasma total cholesterol, i.e., LDL-cholesterol, VLDL-cholesterol,
and HDL-cholesterol, and summarizes the evidence indicating that recommendations
for improved nutrition in the United States--emphasizing sizable reduction in
saturated fat and cholesterol intake, moderate decrease in intake of total fat
and of refined and processed sugars, and of calories for overweight
persons--produce changes in plasma lipidlipoprotein levels that are favorable in
all respects. Finally, it summarizes the findings with respect to the marked
decline in mortality from coronary heart disease, stroke, all cardiovascular
diseases, and all causes in the United States from 1968 to 1978, and presents
evidence indicating that improvements in life style (eating, smoking, and
exercise habits) and control of high blood pressure have contributed
significantly to these trends.
- Language of Publication
- English
- Unique Identifier
- 82232346
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- MeSH Heading (Major)
- Coronary Disease|BL/EP/*ET/PC; Diet|*AE
- MeSH Heading
- Cholesterol|BL; Epidemiologic Methods; Human; Hypertension|CO; Lipids|BL;
Population Surveillance; Risk; Sodium|AE; United States
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0006-341X
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol); 7440-23-5 (Sodium)
Record 136 from database: MEDLINE
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- Title
- Relevance of lipids to heterotransplantation of human malignancies.
- Author
- Perez RL; Mitchell JR; Lozzio BB
- Address
-
- Source
- Oncology, 1982, 39:3, 179-84
- Abstract
- Although the transplantation of human neoplasms in immunodeficient mice is
now a well-established procedure, the majority of primary malignancies cannot be
successfully maintained for long periods of time in adult athymic (nude) and
asplenic-athymic (lasat) mice. Various lipids such as cholesterol, cholesterol
oleate, stearic and palmitic acid esters markedly depress the RES phagocytic
activity and immunocompetence of mammals. In view of the immunosuppressive
properties of certain lipids and in order to graft and grow as many tumors as
possible, further studies into the effects of lipids on the growth of
heterotransplanted human tumors is warranted. Lipids may enhance local growth
and facilitate the development of metastases rarely seen in nude and lasat mice
bearing xenogeneic cancer cells. Lipids may accelerate human malignant cell
proliferation in mice by both depressing further the defense of host and
modifying the cancer cell membrane. The relationship of lipids to the onset and
progression of 'spontaneous' tumors in humans is not known.
- Language of Publication
- English
- Unique Identifier
- 82196395
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document
- MeSH Heading (Major)
- Immunity|*DE; Lipids|*PD; Neoplasms, Experimental|*IM; Phagocytosis|*DE
- MeSH Heading
- Cholesterol|PD; Cholesterol Esters|PD; Dietary Fats; Fatty Acids|PD; Human;
Neoplasm Transplantation; Palmitic Acids|PD; Support, U.S. Gov't, P.H.S.;
Transplantation, Heterologous; Triolein|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0030-2414
- Country of Publication
- SWITZERLAND
- CAS Registry/EC Number
- 0 (Cholesterol Esters); 0 (Dietary Fats); 0 (Fatty Acids); 0 (Palmitic
Acids); 122-32-7 (Triolein); 57-88-5 (Cholesterol)
Record 137 from database: MEDLINE
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- Title
- Dietary lipids and serum cholesterol level: change in diet confounds the
cross-sectional association.
- Author
- Shekelle RB; Stamler J; Paul O; Shryock AM; Liu S; Lepper M
- Address
-
- Source
- Am J Epidemiol, 1982 Apr, 115:4, 506-14
- Abstract
- In the Chicago Western Electric Company study, diet was assessed at the
initial examination, in 1957-1958, of 1900 middle-aged men and again at their
second examination about one year later. At the first examination, lipid
composition of the diet, as summarized by a score based on the formula of Keys,
Anderson and Grande (Grande, F. Predicting change in serum cholesterol from
change in lipid composition of the diet. In: Lauer RM, Shekelle RB, eds.
Childhood Prevention of Atherosclerosis and Hypertension. New York: Raven Press,
1980:145-53), was positively associated with level of serum cholesterol. Between
the first and second examinations, however, hypercholesterolemic men were more
likely than others to have reduced intake of dietary saturated fatty acids and
cholesterol. As a result, at the second examination the cross-sectional linear
association between the diet score and serum cholesterol concentration was
significantly positive for men with initial levels of serum cholesterol less
than 250 mg/dl, significantly negative for men with initial levels of 250 mg/dl
or higher and not significantly different from zero for all men together. The
bias introduced by change in diet among hypercholesterolemic men differs
importantly from bias due to unreliability of measurement and to interindividual
differences in intrinsic level of serum cholesterol, because it can produce
statistically significant but spurious correlations.
- Language of Publication
- English
- Unique Identifier
- 82179532
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Dietary Fats|*ME
- MeSH Heading
- Cross-Sectional Studies|CROSS SECTIONAL STUDIES; Epidemiologic Methods;
Human; Hypercholesterolemia|DH; Illinois; Regression Analysis; Support, Non-U.S.
Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9262
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Dietary Fats); 57-88-5 (Cholesterol)
Record 138 from database: MEDLINE
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- Title
- Atherogenic hyperlipoproteinemia. The cellular and molecular biology of
plasma lipoproteins altered by dietary fat and cholesterol.
- Author
- Mahley RW
- Address
-
- Source
- Med Clin North Am, 1982 Mar, 66:2, 375-402
- Abstract
- Diets high in saturated fat and cholesterol cause alterations in the plasma
lipoproteins, and these alterations cause certain of the lipoproteins to deliver
cholesterol to the cells of the arterial wall. Other changes in lipoprotein are
induced as an attempt to compensate for the delivery of cholesterol to cells.
Atherosclerosis results when influx of cholesterol into the arterial wall
exceeds egress of cholesterol from the tissues. The interactions of the various
plasma lipoproteins are described in order to generate a reasonable hypothesis
characterizing atherogenic hyperlipoproteinemia.
- Language of Publication
- English
- Unique Identifier
- 82171943
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document
- MeSH Heading (Major)
- Arteriosclerosis|*ET; Atherosclerosis|*ET; Cholesterol, Dietary|*AE; Dietary
Fats|*AE; Hyperlipoproteinemia|*ET; Lipoproteins|*BL/PH
- MeSH Heading
- Animal; Apolipoproteins|PH; Cholesterol|ME; Disease Models, Animal; Dogs;
Foam Cells|ME; Human; Lipoproteins, HDL|AN/PH; Lipoproteins, LDL|PH;
Lipoproteins, VLDL|PH; Macrophages|ME; Muscle, Smooth|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0025-7125
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins E); 0 (Apolipoproteins); 0 (Cholesterol, Dietary); 0
(Dietary Fats); 0 (Lipoproteins); 0 (Lipoproteins, HDL); 0 (Lipoproteins, VLDL);
57-88-5 (Cholesterol)
Record 139 from database: MEDLINE
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- Title
- Cholesterol transport between cells and body fluids. Role of plasma
lipoproteins and the plasma cholesterol esterification system.
- Author
- Fielding CJ; Fielding PE
- Address
-
- Source
- Med Clin North Am, 1982 Mar, 66:2, 363-73
- Abstract
- The manner in which cells retain their sterol content is reviewed. Although
most of what is known at the molecular level has been defived from studies in
continuous cell culture, the findings appear to be broadly applicable to
conditions in vivo. The main impetus to this research has come from the
potential direct relevance of cell sterol balance to lipid disorders.
- Language of Publication
- English
- Unique Identifier
- 82171942
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document
- MeSH Heading (Major)
- Body Fluids|*ME; Cholesterol|*ME; Cholesterol Esters|*BL;
Lipoproteins|*BL/PH
- MeSH Heading
- Animal; Biological Transport; Human; Hypercholesterolemia|ME; In Vitro;
Lecithin Acyltransferase|ME; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0025-7125
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 2.3.1.43 (Lecithin Acyltransferase); 0 (Cholesterol Esters); 0
(Lipoproteins); 57-88-5 (Cholesterol)
Record 140 from database: MEDLINE
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- Title
- Colestipol and probucol: treatment of primary and familial
hypercholesterolemia and amelioration of atherosclerosis.
- Author
- Glueck CJ
- Address
-
- Source
- Ann Intern Med, 1982 Apr, 96:4, 475-82
- Abstract
- Colestipol is a safe, effective, cholesterol-lowering, bile-acid sequestrant
that lowers low-density-lipoprotein (LDL) and total plasma cholesterol levels
without consistently affecting high-density-lipoprotein (HDL) cholesterol
levels. Long-term colestipol therapy in conjunction with diet may reduce
xanthoma size, arrest progression of coronary artery atherosclerosis, and may
reduce mortality from coronary heart disease. Probucol, a bisphenol
cholesterol-lowering drug, is an effective cholesterol-lowering agent that
reduces levels of HDL cholesterol, HDL cholesterol, and apoprotein A-1, the
major apolipoprotein of HDL. Because HDL cholesterol is independently and
inversely associated with development of coronary heart disease, the
ramifications of simultaneous lowering of LDL and HDL cholesterol levels by
probucol treatment need further study. Long-term, placebo-controlled studies of
repetitive coronary arteriography, coronary heart disease morbidity and
mortality, or both are needed to ascertain the efficacy of long-term probucol
use in relation to development of atherosclerosis.
- Language of Publication
- English
- Unique Identifier
- 82158596
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document
- MeSH Heading (Major)
- Arteriosclerosis|*DT; Atherosclerosis|*DT; Colestipol|AE/*TU;
Hypercholesterolemia|*DT; Hypercholesterolemia, Familial|*DT; Phenols|*TU;
Polyamines|*TU; Probucol|AE/*TU
- MeSH Heading
- Cholesterol|ME; Drug Therapy, Combination; Human; Nicotinic Acids|TU;
Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0003-4819
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Nicotinic Acids); 0 (Phenols); 0 (Polyamines); 23288-49-5 (Probucol);
50925-79-6 (Colestipol); 57-88-5 (Cholesterol); 59-67-6 (Niacin)
Record 141 from database: MEDLINE
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- Title
- Obesity: does it modulate infectious disease and immunity?
- Author
- Edelman R
- Address
-
- Source
- Prog Clin Biol Res, 1981, 67:, 327-37
- Abstract
- Obesity, high-fat diets, or excess lipids interact with infectious agents
and immunocompetent cells in the following ways: Some infections and autoimmune
diseases are enhanced in inbred mice. In man, surgical wound infections are
increased; the risk of tubercular death is decreased; no data exist on the
interaction of lipids and autoimmune disease. Certain fatty acids and
cholesterol are potent modulators of T lymphocyte and phagocyte functions in
laboratory animals and in leukocyte cultures. However, in humans, the modulation
of immune function by dietary lipids is still uncertain. Precisely how lipids
interact with the immune system opens an important and exciting area for future
research.
- Language of Publication
- English
- Unique Identifier
- 82060535
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document
- MeSH Heading (Major)
- Antibody Formation|*/DE; Dietary Fats|AE/*PD; Hyperlipidemia|CO/*IM;
Infection|*CO; Obesity|CO/*IM
- MeSH Heading
- Animal; Cholesterol|IM; Cholesterol, Dietary|PD; Fatty Acids,
Unsaturated|PD; Human; Immunity, Cellular|DE; Immunosuppressive Agents;
Lipids|ME; Phagocytosis|DE; Structure-Activity Relationship; T-Lymphocytes|IM
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0361-7742
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Cholesterol, Dietary); 0 (Dietary Fats); 0 (Fatty Acids, Unsaturated); 0
(Immunosuppressive Agents); 57-88-5 (Cholesterol)
Record 142 from database: MEDLINE
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- Title
- Lipid measurements for coronary risk assessment: a review.
- Author
- Berg LH
- Address
-
- Source
- Am J Med Technol, 1981 Jul, 47:7, 539-43
- Abstract
- Epidemiological studies have found that high density lipoprotein (HDL)
cholesterol values and low density lipoprotein cholesterol values consistently
correlate with coronary heart disease. In this report, the biochemical
mechanisms by which HDL may help prevent cardiovascular disease are discussed
along with the relationship of HDL to other lipoproteins. The demographic
factors which alter the HDL cholesterol level are identified and possible
clinical implications are considered. Laboratory methods for measuring total
cholesterol, triglyceride, lipoproteins and components of lipoproteins are
summarized. The current role and future implications of these laboratory
procedures in the assessment of coronary heart disease risk are also discussed.
- Language of Publication
- English
- Unique Identifier
- 82021204
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document
- MeSH Heading (Major)
- Coronary Disease|BL/*PC; Lipids|*BL
- MeSH Heading
- Cholesterol|BL; Evaluation Studies; Human; Hyperlipidemia, Familial
Combined|BL; Lipoproteins, HDL|BL; Lipoproteins, LDL|BL; Risk; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0002-9335
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL); 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 143 from database: MEDLINE
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- Title
- Pathogenesis of cholesterol gallstones.
- Author
- LaMorte WW; Matolo NM; Birkett DH; Williams LF Jr
- Address
-
- Source
- Surg Clin North Am, 1981 Aug, 61:4, 765-74
- Abstract
- The factors leading to cholesterol cholelithiasis are probably multiple.
Although the secretion of bile supersaturated with cholesterol seems to be a
common feature among all patients who form cholesterol stones, a variety of
pathophysiologic events can produce an increase in lithogenicity. Dietary
factors, particularly in the grossly obese, lead to an absolute increase in
secretion of cholesterol into bile. Occasionally, excessive loss of the bile
salt pool, for example with regional ileitis, may decrease the ability of bile
salts to solubilize cholesterol. In many other, subtle alterations in the
enterohepatic circulation of bile salts may adversely affect solubility by both
decreasing the secretion of bile salts and increasing the secretion of
cholesterol. Regardless of its cause, supersaturation of bile with cholesterol
appears to be a prerequisite for gallstone formation. However, additional
factors within the gallbladder, such as increased secretion of glycoprotein,
increased absorption of fluids, infection, and stasis, appear to contribute to
the formation of macroscopic stones.
- Language of Publication
- English
- Unique Identifier
- 82017759
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document
- MeSH Heading (Major)
- Cholelithiasis|*ET/ME/PP; Cholesterol|*/ME
- MeSH Heading
- Animal; Bile|ME; Bile Acids and Salts|ME; Crystallization; Enterohepatic
Circulation; Feedback; Human; Liver|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0039-6109
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 57-88-5 (Cholesterol)
Record 144 from database: MEDLINE
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- Title
- Alcohol and high-density lipoprotein cholesterol.
- Author
- Gordon T; Ernst N; Fisher M; Rifkind BM
- Address
-
- Source
- Circulation, 1981 Sep, 64:3 Pt 2, III 63-7
- Abstract
- Associations between alcohol intake and levels of high-density lipoprotein
(HDL) cholesterol were examined in 2473 men and 1530 women seen as part of the
random sample at visit 2 of the Lipid Research Clinics Prevalence Study. More
men than women reported alcohol intake. The alcoholic beverage preference
differed by age and sex. The levels of HDL cholesterol were higher in drinkers
than in nondrinkers. The statistically significant associations varied somewhat
by age; however, the average correlation coefficient was 0.21 for men and 0.25
for women. HDL cholesterol levels were lower in those who reported never
drinking alcohol than in occasional drinkers.
- Language of Publication
- English
- Unique Identifier
- 81259074
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document
- MeSH Heading (Major)
- Alcohol Drinking|*; Cholesterol|*BL; Lipoproteins, HDL|*BL
- MeSH Heading
- Adult; Age Factors; Cross-Sectional Studies|CROSS SECTIONAL STUDIES; Female;
Human; Male; Middle Age; Random Allocation; Sex Factors; Support, U.S. Gov't,
P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL); 57-88-5
(Cholesterol)
Record 145 from database: MEDLINE
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- Title
- Alcohol and high-density lipoprotein cholesterol: causal inference from
diverse study designs.
- Author
- Hulley SB; Gordon S
- Address
-
- Source
- Circulation, 1981 Sep, 64:3 Pt 2, III 57-63
- Abstract
- The association between reported alcohol intake and plasma high-density
lipoprotein (HDL) cholesterol concentration is examined in an effort to
establish whether it was a cause-and-effect basis. A cross-sectional descriptive
study of several populations reveals a strong and consistent dose-response
pattern: Social drinkers have mean HDL cholesterol levels that are higher than
those of teetotalers by as much as 33%. Cross-sectional analyses in another
epidemiological study reveal the association to be independent of potential
confounding factors such as smoking and body weight, and longitudinal analyses
suggest that it is also not a result of certain unmeasured sources of
confounding. A small experiment reveals a 15% reduction in HDL cholesterol
levels among social drinkers who abstain from alcohol from a 2-week period. The
evidence supports the conclusion that alcohol habits are probably one of the
determinants of plasma HDL cholesterol level. A clarification of the relevance
of this phenomenon to clinical medicine awaits future clinical efforts.
- Language of Publication
- English
- Unique Identifier
- 81259073
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document
- MeSH Heading (Major)
- Alcohol Drinking|*; Cholesterol|*BL; Lipoproteins, HDL|*BL
- MeSH Heading
- Cross-Sectional Studies|CROSS SECTIONAL STUDIES; Data Collection; Human;
Male; Questionnaires; Research Design; Risk
- Publication Type
- JOURNAL ARTICLE; REVIEW
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL); 57-88-5
(Cholesterol)
Record 146 from database: MEDLINE
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- Title
- Alcohol intake, cigarette smoking and plasma lipids and lipoproteins in
12--19-year-old children. The Collaborative Lipid Research Clinics Prevalence
Study.
- Author
- Glueck CJ; Heiss G; Morrison JA; Khoury P; Moore M
- Address
-
- Source
- Circulation, 1981 Sep, 64:3 Pt 2, III 48-56
- Abstract
- The relationship of alcohol intake to plasma lipids and lipoproteins was
assessed in 1603 white children, ages 12-19 years, from six Lipid Research
Clinics as part of the Lipid Research Clinics Collaborative Population Studies.
Of the 1603 children, 933 came from a randomly recalled group and 660 from a
group recalled because of elevated cholesterol or triglyceride or both (the
hyperlipidemic recall group). Using multiple regression analysis, the
relationships of lipoproteins (as dependent variables) to alcohol, smoking, age
and body mass (as explanatory variables) are assessed in both recall groups. In
the random recall group, high-density lipoprotein (HDL) cholesterol was
positively related to alcohol intake, independent of the other variables
considered; for every ounce of alcohol intake, HDL cholesterol was 0.55 mg/dl
higher in males and 1.04 mg/dl higher in females. HDL cholesterol was strongly
and inversely related to smoking and body mass in both males and females and was
inversely related to age in males. In females, plasma low-density lipoprotein
(LDL) cholesterol, triglycerides and very low density lipoprotein (VLDL)
cholesterol were all positively related to alcohol intake. In the hyperlipidemic
recall group of children, alcohol intake had a weak positive relationship with
HDL cholesterol in males; in the females, for every ounce of alcohol intake, HDL
cholesterol was higher by 1.5 mg/dl. Alcohol intake was positively related to
triglyceride levels in hypertriglyceridemic male children. In each recall group,
alcohol intake had a small, significant, positive association with HDL
cholesterol levels in 12--19-year-old children, and a less consistent positive
association with triglyceride and VLDL cholesterol. If low HDL cholesterol
concentrations in children are undesirable, attention should first be focused
reduction of smoking (inversely associated with HDL cholesterol) and weight
(inversely associated with HDL cholesterol, positively associated with LDL
cholesterol, triglyceride and VLDL cholesterol), as measures that may modify HDL
cholesterol levels.
- Language of Publication
- English
- Unique Identifier
- 81259072
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document
- MeSH Heading (Major)
- Alcohol Drinking|*; Hyperlipidemia|*EP/ET; Lipoproteins|*BL; Smoking|*
- MeSH Heading
- Adolescence; Adult; Child; Cholesterol|BL; Epidemiologic Methods; Female;
Human; Lipoproteins, HDL|BL; Male; Questionnaires; Sex Factors; Support, U.S.
Gov't, P.H.S.; United States
- Publication Type
- JOURNAL ARTICLE; REVIEW
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, HDL);
57-88-5 (Cholesterol)
Record 147 from database: MEDLINE
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- Title
- HDL-cholesterol: the negative risk factor for coronary heart disease.
- Author
- Tan MH
- Address
-
- Source
- Ann Acad Med Singapore, 1980 Oct, 9:4, 491-5
- Abstract
- High density
