Studies on the mechanism on inhibition of acute alcoholic fatty liver by clofibrate

Abstract

The effect of ethanol on hepatic α-glycerophosphate (α-GP), dihydroxyacetone phosphate (DAP) and triglyceride (TG) concentrations, and on serum levels of triglycerides (TG) and free fatty acids (FFA) was studied 4 and 12 hr after administration of ethanol in normal and ethyl-α-p-chlorophenoxyisobutyrate (clofibrate)-treated rats. In the normal rats, ethanol increased liver α-GP and TG concentrations, α- GP DAP ratio and serum FFA concentration. In the clofibrate-treated rats there was no change in α- GP DAP ratio or α-GP concentration after ethanol, nor was there a significant rise in liver TG concentration. The initial serum TG concentration in the clofibrate-treated rats was about 30% of that in the normal animals. In the normal rats, ethanol administration produced a higher serum TG concentration than glucose, but in the clofibrate-treated rats it did not cause a significant rise in serum TG level. Thus, it appears that clofibrate treatment can inhibit the ethanol-induced change in the hepatic redox state in vivo as in the isolated liver. These results strengthen the view that clofibrate inhibits the production of acute ethanolic fatty liver at least in part by abolishing the ethanol-induced change in the hepatic redox state.