PMID: 8593127Oct 1, 1995Paper

Currently available hypolipidaemic drugs and future therapeutic developments

Baillière's Clinical Endocrinology and Metabolism
J A Farmer, A M Gotto

Abstract

Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing intrahepatic cholesterol, and by increasing the activity of LDL receptors. Nicotinic acid lowers LDL cholesterol and triglyceride by decreasing VLDL synthesis and by decreasing free fatty acid mobilization from peripheral adipocytes. The HMG-CoA reductase inhibitors--fluvastatin, lovastatin, pravastatin and simvastatin--lower LDL cholesterol by partially inhibiting HMG-CoA reductase (the rate-limiting enzyme of cholesterol biosynthesis) and by increasing the activity of LDL receptors. The fibric-acid derivatives--bezafibrate, ciprofibrate, clofibrate, fenofibrate and gemfibrozil--primarily decrease triglyceride by increasing lipoprotein lipase activity and by decreasing the release of free fatty acids from peripheral adipose tissue. Probucol decreases LDL cholesterol by increasing non-receptor-mediated LDL clearance; as an anti-oxidant, probucol also decreases LDL oxidation; oxidized LDL which is thought to lead to atherogenesis. Although ...Continue Reading

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Citations

Mar 17, 2004·The Journal of Nutritional Biochemistry·John D Radcliffe, Dorice M Czajka-Narins
Sep 10, 1999·Clinical Biochemistry·A TheriaultK Adeli
Jan 15, 2011·European Journal of Radiology·M WagnerR Schmitt
May 31, 2012·Chemical Biology & Drug Design·Xiaoyun ZhuWenlong Huang
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Sep 13, 2008·Scandinavian Journal of Gastroenterology·Hasse AbrahamssonPer-Göran Gillberg

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