Origin and Pathogenesis of Fatty Acid Accumulation in the Liver During Prolonged Ethanol Consumption

Abstract

The observation that agents which decrease the normal rate of peripheral fat mobilization prevent or reduce hepatic fat accumulation produced by ethanol has been interpreted to indicate that the primary mechanism responsible for the ethanol induced fatty liver is increased peripheral fat mobilization. A decrease in peripheral fat mobilization however does reduce the overall fat load presented to the liver and may enable this organ to cope with any of the other mechanisms possibly responsible for the development of a fatty liver. Disturbances which lead to a fatty liver in the presence of a normal rate of peripheral fat mobilization may not be capable of producing this when the overall fat load to the liver has been diminished as a consequence of reduction in peripheral fat mobilization. For instance, enhanced mobilization of adipose fatty acids is not the primary defect by which ethionine produces steatosis, yet glucose, by inhibiting peripheral fat mobilization, reduces the ability of ethionine to induce the fatty liver (CAMPAGNARI-VISCONTI, L. et al., 1962).Thus effects of inhibition of fat mobilization are difficult to interpret.