Earlier studies showed that the
fatty liver, caused by feeding rats the Lieber-DeCarli alcohol diet for four weeks, was prevented if the diet was supplemented with
dihydroxyacetone (22 g/l),
pyruvate (22 g/l) and
riboflavin (2.2 g/l). In the present study, we observed that
fatty liver was prevented if the alcohol diet was supplemented with
glycerol and
lactate (22 g/l each) and
riboflavin (2.2 g/l). Hence, the prevention of
alcoholic fatty liver by the dietary supplementation with
dihydroxyacetone and
pyruvate may not be related to their capacity to serve as
hydrogen acceptors and to oxidize
NADH produced during
ethanol metabolism. When rats were fed the alcohol diet supplemented with either
glycerol or
pyruvate, the hepatic
triglyceride (TG) levels were similar to those in rats pair-fed a Lieber-DeCarli control diet in which alcohol was replaced with an isocaloric amount of
dextrins. Therefore, the prevention of
fatty liver does not require the simultaneous presence of several supplements. Dietary
dihydroxyacetone or
riboflavin did not reduce
alcoholic fatty liver. Supplementation of the
ethanol diet with isocaloric amounts of
lactate or
glucose, instead of
pyruvate, did not abolish the development of
fatty liver but caused a marked reduction in the hepatic TG levels. Animals fed the alcohol diet consumed only small amounts of
carbohydrate for long periods of time. Since the inclusion of
glucose or its metabolites in the alcohol diet fed to rats caused a marked decrease in the liver TG content, it is likely that the production or prevention of
fatty liver is related to carbohydrate metabolism.