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American Journal of Clinical Nutrition, Vol 23, 474-478, Copyright © 1970 by The American Society for Clinical Nutrition, Inc.
1 From the Section of Liver Disease and Nutrition, Bronx Veterans Administration Hospital, and the Department of Medicine, Mt. Sinai School of Medicine of the City University of New York, New York, New York
To assess the quantitative relationship between fat content of the diet and lipid accumulation in the liver after alcohol ingestion, rats were given various isocaloric liquid diets, containing 18% of total calories as protein and 36% as ethanol or isocaloric carbohydrate. The remainder of the calories consisted of varying amounts of fat (2, 5, 10, 15, 25, 35, or 43% of total calories) and corresponding amounts of carbohydrate. Dietary fat consisted of ethyl linoleate (2% of total calories), to avoid essential fatty acid deficiency, and an olive-corn oil mixture. After 24 days of ethanol and 43% of calories as fat, hepatic triglycerides increased seven- to eightfold. With 35% of calories as fat, the increase was fivefold and with 25%, only two- to threefold. No significant decrease in hepatic lipid accumulation was achieved by further reduction in the dietary fat; a diet with 25% of calories as fat (about half that of the average United States diet) appears, therefore, to be optimal for minimizing the steatogenic effects of ethanol.
An excess of dietary protein did not affect the ethanol-induced steatosis, and even a combination of a high protein-low fat diet did not achieve full protection against the ethanol-induced hepatic deposition of lipids in the liver. The ethanol effect persisted unchanged for periods up to 3-5 months.
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