Studies on modification of alcoholic liver disease by dietary carbohydrate and fat

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The effects of dietary carbohydrate (CHO) level on lipid peroxidation caused by ethanol were investigated in rat liver. Ethanol treatment enhanced microsomal ethanol oxidation, which was potentiated by lowered CHO intake. Ethanol administration markedly increased lipid peroxidation and triglyceride content in the liver of rats fed with low-CHO diet, and slightly in rats fed with high-CHO diet: lipid peroxidation and triglyceride accumulation caused by ethanol were potentiated by low-CHO diet. Liver glutathione content was decreased not by ethanol intake but by lowered CHO intake. These results suggest that lowered-CHO intake involves in the development of ethanol-induced hepatic damage in rats.In order to investigate the effect of CHO intake on ethanol induced hepatic damage, liver function, frequencies of various food and alcohol intakes were surveyed in 2165 healthy men aged from 18 to 85 living in Nagano Prefecture. Serum gamma-glutamyl transpeptidase (gamma-GTP), glutamic-oxaloacetic transaminase(GOT), glutamate pyruvic transaminase(GPT) activities, ratio of GOT to GPT, triglyceride and HDL-cholesterole increased with increasing ethanol consumption. In contrast, the ratio of HDL to LDL de creased with increasing ethanol consumption. The intake of CHO clearly decreased with increasing ethanol consumption, but the intake of fat and protein not found to increase or decrease evidently following ethanol consumption. With ethanol intakeadjusted analysis, lowered- CHO intake may potentiate ethanolinduced increase in serum -GTP activity. We deduced that CHO intake contributes to l-induced hepatic damage.