Relation of Ethanol Inhibition of Hepatic Fatty Acid Oxidation to Ethanol-Induced Fatty Liver

Abstract

Summary

The quantitative importance of the inhibition of hepatic fatty acid oxidation for the pathogenesis of ethanol fatty liver has been investigated in perfused rat livers. Advantage has been taken of the fact that octanoate is poorly esterified in rat liver. Thus, by using octanoate the effects of ethanol on hepatic fatty acid esterification can be separated from effects on fatty acid oxidation. Comparison of the effect of ethanol perfusion on the metabolism of octanoate-[1-¹⁴C] and palmitate-1[-¹⁴C] indicated that ethanol decreased fatty acid oxidation to CO₂ for both acids. However, in contrast to the palmitate data, inhibition of the oxidation of octanoate to CO₂ did not lead to an increase in the recovery of ¹⁴C from octanoate in the liver. Ethanol inhibition of CO₂ production from fatty acids did not of itself lead to an accumulation of fatty acids in the liver. Thus, the data suggest that ethanol inhibition of CO₂ production from fatty acids does not contribute to the accumulation of fatty acids (in the form of triglycerides) seen in livers from ethanol treated rats.