On the mechanism of ethanol-induced accumulation of triglycerides in the liver

The possibility that ethanol or acetaldehyde has a direct effect on the activity of acyl-CoA-ligases or sn -glycerophosphate acyltransferases or on the biosynthesis of phosphatidic acid and triglycerides from free fatty acids was studied with subcellular preparations from rat liver. No stimulatory effect of ethanol or acetaldehyde could be observed in any case. It was further shown that the microsomal fraction of homogenate of livers of rats treated with ethanol (single peroral dose of 4.5 g of ethanol per kg body weight) did not have an increased capacity to biosynthesize phosphatidic acid. The possibility was excluded that excess cofactors necessary for formation of phosphatidic acid are responsible for the higher accumulation of triglycerides in livers of rats treated with ethanol. The results indicate that the increased formation of triglycerides in liver of rats treated with ethanol is not due to increased activity of acyl-CoA-ligase or sn -glycerophosphate acyltransferase or due to increased availability of sn -glycerophosphate, ATP or CoA-SH. It is suggested that increased availability of fatty acids is the major explanation for the increased accumulation of triglycerides in the liver after ethanol administration.