[Triglyceride synthesis and oleic acid catabolism by hepatic microsomes and mitochondria in clofibrate or procetofen-treated rats].

Several studies have explained the influence of clofibrate on lipid metabolism, and the depressive effect of this drug on blood triglyceride and cholesterol levels is now well-known. Inhibition of triglyceride formation in the liver, and thus a reduced release of newly synthesized triglycerides coupled with increased fatty acid catabolism, might partially explain the lipid-lowering effect of clofibrate. These in vitro studies were designed to determine the effects of a new normolipemic product, procetofen, on hepatic microsomal synthesis of triglycerides and mitochondrial catabolism of oleic acid. These subcellular particles were isolated from normal rats or those treated for 8 days with clofibrate (250 mg/kg/day) or procetofen (100 mg/kg/day). Microsomal triglyceride synthesis from 3H oleate was not significantly changed in the clofibrate-treated group, while it decreased by 25 p. 100 in the procetofen-treated group. In the mitochondrial system, 14CO2 production from 10-14C oleate was small and unaffected by either drug. Therefore, the radioactivity of acid-soluble products was enhanced by 40 or 130 p. 100 when mitochondria were isolated from the livers of rats treated with clofibrate or procetofen, respectively. These data support the hypothesis that the plasma lipid-lowering effect of procetofen in vivo could be explained by increased hepatic fatty acid degradation which probably induced a reduction of triglyceride synthesis.