Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of simvastatin (MK-733), an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, on plasma triacylglycerol (TG) levels was studied in rats. Dietary administration of MK-733 (0.055%, w/w) for 7 days significantly (P less than 0.05) reduced plasma TG levels by 30.6% associated with a 44.3% significant (P less than 0.01) reduction in very low density lipoprotein TG (VLDL-TG) as compared to those in the concurrent control rats. Clofibrate (0.08%, w/w) also significantly (P less than 0.05) decreased plasma TG levels by 26.1%. MK-733 did not affect the triacylglycerol secretion rate (TGSR) during 0-1.5 hr after administration of Triton WR-1339, but reduced it by 33.9% during 1.5-3.0 hr. Clofibrate also decreased TGSR during 1.5-3.0 hr. MK-733 increased lipoprotein lipase (LPL) activity in epididymal adipose tissue and thigh muscle by 36.3 and 55.0% respectively. MK-733 significantly (P less than 0.05) increased LPL activity in the post-heparin plasma by 21.5%, although it did not affect hepatic triacylglycerol lipase (H-TGL) activity. Clofibrate did not affect LPL activity in the tissues or LPL and H-TGL activities in the post-heparin plasma. It is considered that the mechanism of plasma TG-lowering effect of MK-733 is the removal of VLDL-TG by an increase in LPL activity in the tissues as well as a decrease in the TGSR.
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PMID:Effect of simvastatin (MK-733) on plasma triacylglycerol levels in rats. 200 92

Anthropometric data, plasma lipoprotein lipid levels, and post-heparin lipoprotein lipase (PHLPL) activity were measured in nine patients with type III hyperlipoproteinemia (HLP) and two hypocholesterolemic subjects with the apo-E2/2 phenotype. Five type III HLP patients were treated with clofibrate. Log PHLPL activity was inversely correlated (r = -0.667, p less than 0.05) and age was positively correlated (r = 0.706, p less than 0.05) with cholesterol levels in the VLDL fraction of plasma from type III HLP patients. The correlation between log PHLPL and VLDL cholesterol levels remained significant when age was held constant in partial correlation analysis. Together age and log PHLPL activity accounted for 77% of individual variation in VLDL cholesterol levels in the type III patients. Clofibrate treatment raised PHLPL activity (+48%, p less than 0.05) and reduced the levels of VLDL cholesterol (-67%, P less than 0.05), VLDL triglycerides (-40%, P less than 0.02), and the ratio cholesterol/triglyceride in VLDL (-50%, P less than 0.05) in five type III HLP patients. Mean PHLPL activity was higher in the hypocholesterolemic subjects with the apo-E2/2 phenotype compared to the type III HLP patients. These results suggest that lipoprotein lipase activity and factors associated with age modulate the levels of abnormal and atherogenic remnant particles (beta-VLDL) in the VLDL plasma fraction of type III HLP patients.
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PMID:Cholesterol in the plasma very low density lipoprotein fraction in patients with type III hyperlipoproteinemia: analysis of factors which modulate its concentration. 316 1

Ten male, normolipaemic, non-obese subjects were given clofibrate 2 g daily, fenofibrate 300 mg daily, bezafibrate 600 mg daily and probucol 1 g daily for eight days, in a crossover study with a wash-out period of 4-8 weeks between each drug regimen. Clofibrate, fenofibrate and bezafibrate caused a significant decrease in serum triglycerides, total cholesterol and LDL-cholesterol concentrations. Probucol caused a significant increase in serum LDL-cholesterol concentration. Serum HDL-cholesterol concentration was significantly increased by bezafibrate and significantly decreased by probucol. All drugs but probucol led to a significant rise in the activity of the plasma lipoprotein lipase; there was not a significant increase in the activity of plasma hepatic lipase after any drug. The activity of plasma lecithin: cholesterol acyltransferase was significantly increased by fenofibrate and probucol. Analysis of the correlations between serum lipids and plasma lipolytic enzymes suggests that the mechanism of the hypolipidaemic action of clofibrate and bezafibrate might be related to increased catabolism of triglyceride-rich particles; that of fenofibrate and probucol was less clear and might be multifactorial in origin.
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PMID:Effects of clofibrate, bezafibrate, fenofibrate and probucol on plasma lipolytic enzymes in normolipaemic subjects. 661 25

Clofibrate treatment decreased drastically the activity of serum postheparin lipoprotein lipase of rats fed with fat-free test diet but had no effect on hepatic lipase. 3 weeks' treatment was followed by a significant fall in serum cholesterol caused by a marked decrease in HDL-cholesterol. Clofibrate decreased in vitro synthesis of cholesterol and fatty acids in jejunal villous cells but not in the crypt cells.
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PMID:Clofibrate decreases jejunal cholesterol synthesis and activity of postheparin plasma lipoprotein lipase in the rat. 685 70

1. The effects of KRN4884, a novel pyridinecarboxamidine type KATP channel opener, on serum triglyceride levels were investigated in Sprague-Dawley rats. 2. Oral administration of KRN4884 (3 mg kg-1) for 10 days caused a significant reduction in serum triglyceride levels, which was comparable to that of clofibrate (160 mg kg-1). Reduction in serum triglyceride levels by KRN4884 and clofibrate were accompanied by a reduction in triglyceride levels both in chylomicron and in very low density lipoprotein. KRN4884 treatment did not affect serum concentrations of total cholesterol and phospholipid, but did increase free fatty acid levels. Clofibrate reduced total cholesterol, phospholipid and free fatty acid levels. 3. Administration of clofibrate significantly decreased triglyceride secretion rate as measured by the Triton WR-1339 injection procedure, while KRN4884 did not. 4. Rats receiving KRN4884 exhibited an increase in lipoprotein lipase (LPL) activity both in adipose tissue and in skeletal muscle. There was an inverse correlation between serum triglyceride levels and tissue LPL activities. KRN4884 did not change hepatic triglyceride lipase (HTGL) activity. Clofibrate affected neither LPL nor HTGL activities. 5. It is concluded that administration of KRN4884 results in reduced serum triglyceride levels which may be due to the enhancement of LPL activity in peripheral tissues.
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PMID:Effects of KRN4884, a novel pyridinecarboxamidine type KATP channel opener, on serum triglyceride levels in rats. 911 67

This study investigated the effects of clofibrate treatment on blood lipids, hepatic enzyme activities and relative expression of genes involved in lipid metabolism of grass carp fed with high non-protein energy diets. For that purpose, five diets were formulated: a commercial-like diet (Control), a high-carbohydrate diet (HC), a high-fat diet (HF) and two diets identical to the HC and HF diets, but supplemented with 1.25 g kg(-1) clofibrate (HC + Clo and HF + Clo diets). Grass carp fed the HC and HF diet exhibited increases in blood lipids and body fat compared with the control group after 4 weeks. In the clofibrate treatment groups, there was a marked decrease in triacylglycerol and cholesterol concentrations of plasma, and total lipids of the whole body, mesentery adipose tissue and liver tissue. Fish treated with clofibrate exhibited increased hepatic acyl-CoA oxidase activity, but did not show any changes in carnitine palmitoyltransferase (CPT) I activity compared with HC and HF diets without clofibrate. Clofibrate treatment had no effect on peroxisome proliferator-activated receptor alpha and CPT I mRNA expression. However, there was an increase in lipoprotein lipase expression in the clofibrate-treated groups. In addition, the relative mRNA expression levels of hepatic de novo lipogenic enzymes (fatty acid synthetase and acetyl coenzyme-A carboxylase) were significantly higher in the fish fed the HC diet than those of other groups, and clofibrate inhibited this increase. These results suggest that clofibrate has the hypolipidaemic effects and affects lipid metabolism in grass carp.
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PMID:Effects of lipid-lowering pharmaceutical clofibrate on lipid and lipoprotein metabolism of grass carp (Ctenopharyngodon idellal Val.) fed with the high non-protein energy diets. 2521 89