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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male Sprague-Dawley rats were maintained on cholesterol and garlic oil for 12 weeks. Cholesterol induced hyperlipidemia was controlled by garlic feeding. Garlic treatment did not alter the concentrations of circulating thyroid hormones and thyroidal uptake of radioiodine. The results indicate that the hypolipidemic effect of garlic is probably not mediated through the thyroid.
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PMID:Hypolipidemic effect of garlic and thyroid function. 651 87

Hyperlipidemia is common in diabetic patients. While our understanding of lipid and lipoprotein metabolism in diabetes is incomplete, a pathophysiologic approach to this problem is presented. It is based on the recognition that diabetes is metabolically heterogeneous. Thus the roles of insulin deficiency, insulin resistance, obesity, and genetic factors are discussed in relation to their effects on lipoprotein production and catabolism. The most important defect in insulin-deficient subjects appears to be a deficiency of lipoprotein lipase, which is responsible for the removal of the triglyceride-rich lipoproteins. In non-insulin-dependent subjects there is evidence for a removal defect as well as, in some patients, for overproduction of VLDL-triglyceride. Cholesterol levels may be elevated and it is important to distinguish between VLDL, LDL, and HDL as the causes for these increases. HDL-cholesterol levels may be increased in insulin-dependent subjects, whereas they may be decreased in obese non-insulin-dependent patients. Mild elevations of LDL-cholesterol may occur in inadequately controlled type I and II diabetic patients, while elevated VLDL may raise the serum cholesterol in addition to the triglyceride levels. The rationale for therapy is based on the complications of severe hypertriglyceridemia and the risk of occlusive atherosclerosis. Management is directed at improving glycemic control, altering dietary composition, and reducing calories in obese patients. Improved glycemic control is effective in reducing triglyceride and cholesterol levels in insulin-deficient subjects. The response of the non-insulin-dependent diabetic patient to improved control may be complicated by associated obesity or familial hyperlipidemia. The advantages and disadvantages of fat versus carbohydrate restriction in the diet are discussed. Finally, resistant hyperlipidemia may require drug therapy. Diabetic hyperlipidemia should be viewed as resulting from an interaction between the diabetic syndrome, the genetic background of the patient, and the environment.
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PMID:Lipid disorders in diabetes. 675 32

Cholesterol esterification, cholesteryl ester transfer between lipoproteins, and cholesterol transport between lipoproteins and cultured cells have been measured in the plasma of 22 patients with primary hyperlipidemia and 10 normolipidemic subjects. In hyperbetalipoproteinemia, increase in plasma low density lipoprotein levels was associated with a reduction of cholesteryl ester transfer rates, and with a reversal of the normal direction of sterol transport between fibroblasts and their plasma culture medium. Instead of net transport from cells to medium there was a net uptake of sterol from plasma by the cells, despite a level of plasma lecithin/cholesterol acyltransferase activity that was within the normal range. In dysbetalipoproteinemia, esterification rates were increased above normal levels, but cholesteryl ester transfer was reduced and the direction of sterol transport between the cells and plasma medium was reversed, as in the hyperbetalipoproteinemic group. In hypertriglyceridemia, those subjects with cardiovascular disease showed a metabolic pattern similar to the hyperbetalipoproteinemic group. The subjects in this group without symptoms of cardiovascular disease showed a normal direction of sterol transport, normal or raised rates of cholesteryl ester transfer between lipoproteins, and an increased rate of sterol esterification in plasma that decreased towards normal levels as plasma triglyceride levels decreased. Despite their quite distinct metabolic patterns there was no consistent difference between the two hypertriglyceridemic groups in triglyceride or cholesterol levels, very low density lipoprotein composition, or electrophoretic or isoelectric focussing patterns. All hypertriglyceridemic subjects with documented cardiovascular disease showed reversed cell-plasma sterol transport and all subjects without such disease showed a normal direction of cell-plasma sterol transport. The results of this study indicate major and reproducible abnormalities in plasma cholesterol metabolism in several groups of subjects with genetically distinct hyperlipidemias, who are at risk for atherosclerotic vascular disease. The possible predictive value of sterol metabolic measurements in the analysis of cardiovascular disease is discussed.
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PMID:Cholesterol net transport, esterification, and transfer in human hyperlipidemic plasma. 682 17

Hyperlipidemia was induced in rats by feeding them cheese mixed with high levels of cholesterol. Triglyceride levels more than doubled from 70.4 +/- 25.8 mg/dl before the diet to 160.1 +/- 50.5 mg/dl three weeks after initiation of the diet, and cholesterol levels were increased by approximately 25% from 72.5 +/- 8.1 mg/dl to 98.9 +/- 18.5 mg/dl after three weeks of the diet. The effects of microsurgically created side-to-side and end-to-side portacaval shunts were then studied. Triglyceride levels were lowered to normal after either type of shunt (68.4 +/- 19.2 mg/dl in the side-to-side group and 58.1 +/- 25.7 mg/dl in the end-to-side group) by four weeks after the creation of the shunt. Cholesterol levels tended to be slightly lower after either type of portacaval shunt, but did not return to normal. The mechanism by which the portacaval shunt reduced elevated triglyceride levels and, to a lesser extent, cholesterol levels is not clear, but hyperlipidemia induced by a high cholesterol diet in rats should be a useful model for further study of this question.
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PMID:The effect of portacaval shunt on hyperlipidemia in rats. 696 9

Hypothyroid rats fed an atherogenic diet (A) for 3 weeks developed a marked hyperlipidemia characterized by elevated very low density lipoprotein (VLDL) and low density lipoprotein (LDL) cholesterol. Cholesterol concentrations of adipose tissue, liver, carcass and soleus muscle were significantly increased in rats fed the A diet versus rats fed a control diet (C). After 5 months on the A diet, cholesterol concentrations of adipose tissue, carcass and soleus muscle were not different from those measured in rats fed the A diet for 3 weeks; however, liver cholesterol concentration was 20-fold higher. To study the mechanisms by which the A diet increased adipocyte cholesterol content, in vitro binding studies were conducted with normal (N) and cholesterol enriched (CH) 125I-labeled VLDL. The inability of unlabeled N and CH VLDL to displace 125I-labeled VLDL supports the concept that VLDL was not specifically bound by rat adipocytes. The observation that adipocyte and other tissue cholesterol levels were similar at 3 weeks and 5 months suggests regulation of tissue cholesterol concentrations. The mechanism of regulation of adipocyte cholesterol was not related to VLDL binding or differential binding rates between N and CH VLDL.
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PMID:Studies on the etiology of increased tissue cholesterol concentration in cholesterol-fed hypothyroid rats. 714 14

Efficacy of 1-(theophyllin-7-yl)-ethyl-2-[2-(p-chlorophenoxy)-2-methylpropionate] (etofylline clofibrate, ML 1024, Duolip) and its molecule components (metabolites) of structurally similar theophylline esters and of clofibrate as standard was investigated in the artificial hyperlipidaemia of the rat. In accordance with former results etofylline clofibrate was antilipaemically active and, in contrast to similar esters and clofibrate, significantly decreased the cholesterol level. An investigation of the efficacy of its metabolites, either alone or in equivalent mixture, as well as of the standard clofibrate under fat diet demonstrated low efficacy of etofylline, but an increased activity in combination with clofibrate or clofibric acid. The activity of the combination is significantly superior to that of clofibrate under fat diet, but not under normal diet. The increased efficacy of etofylline clofibrate is undoubtedly an unusual potentiation, an additive effect of the metabolites can be excluded. Cholesterol and triglycerides are relevant parameters for the experimental evaluation of the efficacy. Measurement of total lipids offers no additional information. Substitution of triglycerides by total-beta-lipoproteins as parameter seems methodically useful, since values of cholesterol, triglycerides and beta-lipoproteins correlate well under normal diet.
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PMID:[Evaluation of the antilipaemic potential of etofylline clofibrate, its metabolites and clofibrate in dietary-induced hyperlipidaemia in the rat (author's transl)]. 719 56

Experimental hyperlipemia induced by a high cholesterol diet (HCD) in male Sprague-Dawley rats was investigated by measuring lipid levels in serum, liver and aorta. For old rats were fed a laboratory chow diet containing 0.5, 1.0 and 2.0% of cholesterol, for 6 weeks. Serum total lipid (TL) and total cholesterol (TC) in 1.0% HCD were markedly increased and reached peaks by feeding HCD for 18 to 21 days. Although the degree of increase in serum TL and TC was similar in both 0.5 and 2.0% HCD groups, these levels decreased more rapidly in the former and more slowly in the latter, after the levels had been reached a peak. The serum free cholesterol level reached a peak in those fed 0.5% HCD for 12 days and those fed 1.0% HCD for 21 days, but the subsequent reduction was smaller in extent as compared with serum TL and TC. Serum phospholipid (PL) level reached a peak in those fed both 0.5 and 1.0% HCD groups for 12 days and this level was maintained until 42 days in the 1.0% HCD group. Serum triglyceride (TG) levels increased during the first half of the experimental period, but decreased in the second half, with no significant difference between the 0.5 and 1.0% HCD groups. Cholesterol in high density lipoprotein (HCD-C) decreased in rats on the HCD and there was a tendency toward reversion to normal levels from the 4th week in the group on the 2.0% diet, however, a continual decrease occurred in the 0.5 and 1.0% groups. The change in phospholipid in HDL (HDL-PL) was similar to that of HDL-C in both the 0.5 and 1.0% HCD groups. In liver lipids, TL and TC were markedly increased by HCD, but TG increased at first and then decreased as did serum TG. Liver PL decreased by 0.5 and 1.0% HCD groups. In aorta lipids, TL and TC decreased. As a remarkable increase in serum lipids and decrease in HDL-C and HDL-PL were continuous in the 1.0% HCD in comparison with 0.5 or 2.0% HCD, 1.0% HCD appears to be the most suitable experimental model of hyperlipemia in rats. In addition, it is considered that 0.5% HCD is suitable for investigation of the effect of a drug for a relatively short period of treatment.
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PMID:[Variation of lipids in rats fed a cholesterol diet (author's transl)]. 731 99

1) In two patient with excessive hyperlipidemia diet in the post-partum days resulted in a rapid reduction of the high neutral fats in the serum which were 6,150 mg/dl and 6,290 mg/dl respectively. In one patient the hyperlipidemia was reduced by diet during the pregnancy. The course of the pregnancies and the puerperium were uneventful. Complications during delivery were not related to the hyperlipidemia. Coagulation defects were not tested.--2) Excessively high serum lipid values of the mother only had a minor influence on the serum lipid values of the mother only had a minor influence on the serum lipid values of the infants. The infants had slightly elevated values compared to controls. One infant was tested at age 7 months and showed definitely elevated lipids with higher values than neonatally. A familial hyperlipidemia was confirmed in this case.--3) The milk fat values (Total Cholesterol and Neutral fats) were not influenced by the hyperlipidemia. Breast feeding was therefore safe.--4) Both infants of the mothers with hyperlipidemia had neonatal hyperbilirubinaemia with values of maximal 16.2 mg% and 16.7 mg% which required phototherapy.
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PMID:[Excessive hyperlipidemia during pregnancy (author's transl)]. 740 9

Little is known about the relationships between hyperlipidemia and bile acid metabolism. However, hypolipidemic treatment with fibric acid derivatives has been shown to increase biliary cholesterol secretion, presumably by reducing bile acid synthesis. To clarify such relationships, we investigated the effects of different hyperlipoproteinemic conditions and of treatment with fibric acid derivatives on the rates of cholesterol 7 alpha-hydroxylation (the limiting step of bile acid synthesis) in humans. We studied 10 patients (aged 36 to 68 years) with lipoprotein phenotype IIa and with a clinical diagnosis of heterozygous familial hypercholesterolemia, a condition of reduced activity of LDL receptors, and 11 patients (aged 48 to 70 years) with lipoprotein phenotype IIb or IV and clinical diagnosis of familial combined hyperlipidemia, a condition probably related to increased hepatic lipoprotein synthesis. Cholesterol 7 alpha-hydroxylation rates were assayed in vivo by tritium release assay after an intravenous injection of [7 alpha-3H]cholesterol. The results were compared by ANOVA to the values obtained in a group of 28 normolipidemic patients (aged 34 to 83 years), with age as the covariate. Six patients were also studied after treatment with gemfibrozil (900 to 1200 mg/d for 6 to 8 weeks) and 5 patients were studied after treatment with bezafibrate (400 mg/d for 6 to 8 weeks). Hydroxylation rates were 0.82 +/- 0.22 mmol/d in the familial hypercholesterolemia group and 1.30 +/- 0.47 mmol/d in the familial combined hyperlipidemia group (P < .05 between the two groups and between patients with familial combined hyperlipidemia and control subjects; P = NS between patients with familial hypercholesterolemia and control subjects, as determined by ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of different phenotypes of hyperlipoproteinemia and of treatment with fibric acid derivatives on the rates of cholesterol 7 alpha-hydroxylation in humans. 762 97

In Jan. 1994, The ROC Society of Internal Medicine and the International Lipid Information Bureau, Taiwan (ILIB, Taiwan) jointly announced national guidelines for the diagnosis and management of lipid disorders. This guideline review the scientific basis and strategies for coronary artery disease (CAD) prevention. This guidelines were developed by an experts panel with various scientific backgrounds. Both two recent publications, the International Task Force and European Atherosclerosis Society (EAS) in 1992 and Adult Treatment Panel II (ATP II) from the National (USA) Cholesterol Education Program (NCEP), were adopted and modified. This guideline covered basic metabolism of lipoprotein, detection method of lipoprotein analysis, coronary risk factors, managements of dyslipidemia, goal of therapy and local epidemiological data. In this guidelines, lipid disorders are classified into hypercholesterolemia (serum cholesterol > 200 mg/dL), combined hyperlipidemia (serum cholesterol > 200 mg/dL and triglyceride > 200 mg/dL) and hypertriglyceridemia (serum triglyceride > 200 mg/dL). In the absence of CAD and with less than two risk factors, target levels for LDL-cholesterol should be < 160 mg/dL; with more than two risk factors, < 130 mg/dL; in the presence of CAD, 100 mg/dL. In individuals with hypertriglyceridemia the target levels for triglyceride are 200 mg/dL. Secondary prevention of CAD is considered as one of the most important issue. Two generalized modalities are recommended to achieve the goal, i.e., non-pharmacological therapy which include weight reduction, regular exercise, smoking cessation, life style modification and pharmacological therapy. It is hoped that this guideline could help medical personnels dealing with patients with dyslipidemia and eventually, reduce the occurrence of CAD in Taiwan.
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PMID:Summary of the national guidelines for the diagnosis and management of lipid disorders in Taiwan. The experts panel. 771 90


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