Hepatic triacylglycerol accumulation induced by ethanol and carbon tetrachloride: interactions with essential fatty acids and prostaglandins

Abstract

Triacylglycerol accumulation in the liver (fatty liver) caused by ethanol or carbon tetrachloride involves interactions with essential fatty acids and prostaglandins. The degree to which the fatty liver develops is dependent on total dietary fat intake. Both ethanol and carbon tetrachloride impair desaturation of linoleic acid and dihomo-gamma-linolenic acid and this appears to be relevant to the pathogenesis of fatty liver from two points of view. First, low arachidonic acid in liver phospholipids is associated with increased liver triacylglycerol content whether caused by ethanol, carbon tetrachloride, or essential fatty acid deficiency. Second, essential fatty acids including gamma-linolenic acid and arachidonic acid, as well as the prostaglandins, prevent ethanol- and carbon tetrachloride-induced fatty liver. Arachidonic acid and possibly the prostaglandins are therefore likely to be directly involved in lipoprotein and triacylglycerol secretion by the liver.