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Write To Karl Loren Table Of Contents

200 Different Cholesterol Studies
From 1988 to
Life Flow One
The Solution For Heart Disease

by
Karl Loren


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Links To Scientific Studies About Choesterol
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Links To Scientific Studies About Cholesterol
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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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