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Wiley InterScience | ||||||||
  Clinical and Experimental Pharmacology and PhysiologyVolume 22 Issue s1, Pages S313 - S315 Published Online: 28 Jun 2007 Journal compilation © 2010 Blackwell Publishing Asia Pty Ltd
Abstract | References | Full Text: PDF (Size: 305K) | Related Articles | Citation Tracking  LIPID-REGULATING ACTION OF GEMFIBROZIL IN THE STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RAT Copyright 1995 Blackwell Publishing Asia Pty Ltd KEYWORDS apolipoproteins • cholesterol diet • gemfibrozil • high density lipoprotein • lipoprotein lipase • lipoprotein metabolism • stroke-prone spontaneously hypertensive rat • trigly-ceride lipase ABSTRACT
1. Gemfibrozil (Lopid®) is extensively used as lipid-regulating agent in the Western World, and its beneficial effect is demonstrated in human studies such as the Helsinki Heart Study. However, the mechanism of its hypolipidaemic action is not fully understood. In the present paper, to elucidate the hypolipidaemic mechanism, we examined the effects of gemfibrozil on lipid metabolism in the normocholesterolaemic and hypercholesterolaemic stroke-prone spontaneously hypertensive rat (SHRSP). 2. Gemfibrozil effectively increased high density lipoprotein (HDL) subfraction rich in apoE (apoE-HDL) and significantly decreased very low density lipoprotein (VLDL) in normocholesterolaemic SHRSP. In the liver of normocholesterolaemic SHRSP, gemfibrozil significantly reduced the activity of micro-somal acyl-CoA: cholesterol acyltransferase. 3. Gemfibrozil markedly reduced atherogenic & very low density lipoprotein (β-VLDL) and low density lipoprotein (LDL) in hypercholesterolaemic SHRSP fed a high-fat and high-cholesterol diet (HFC diet). On the other hand, it significantly increased the contents of apoA-I, A-IV and E in the HDL fraction compared with the control group, suggesting that gemfibrozil effectively increases anti-atherogenic HDL subfractions rich in apoA-I, A-IV or E. In the liver of hypercholesterolaemic SHRSP, gemfibrozil markedly prevented lipid accumulation. Accepted for publication 10 July 1995. | 
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