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Journal of Lipid Research, Vol. 10, 283-287, May 1969
Cornell Medical Division, Bellevue Hospital, New York 10016; Department of Medicine, Cornell University Medical College, New York 10021; Section of Liver Disease and Nutrition, Bronx V.A. Hospital, Bronx, New York 10468; and Department of Medicine, Mt. Sinai School of Medicine, New York 10029
In a study of the pathogenesis of hepatic fat accumulation under experimental conditions mimicking chronic alcoholism, rats were fed a low-fat diet, deficient in amino acids and choline, containing either ethanol or isocaloric amounts of carbohydrate. Dietary deficiencies alone produced a moderately fatty liver after 24 days. The combination of ethanol and dietary deficiencies resulted in enhanced lipid accumulation, which was apparent after only 11 days. In an investigation of the origin of hepatic triglyceride fatty acids, the experiment was repeated after the adipose lipids had been marked by the feeding of oils containing characteristic fatty acids (linseed oil, containing linolenate, or coconut oil, containing laurate and myristate). In all animals, the fatty acid composition of the hepatic triglycerides differed markedly from that of adipose tissue; it had a larger percentage of endogenously synthesized fatty acids and a five times smaller percentage of the marker fatty acids. In addition, ethanol feeding resulted in a greater retention of the marker fatty acids in the adipose tissue. Thus, the deposition of hepatic triglycerides produced by the feeding of deficient diets is markedly potentiated by ethanol; the triglyceride fatty acids accumulated under these conditions appear to originate, for the most part, not from mobilization of depot fat, but from endogenous synthesis. Supplementary key words adipose tissue choline lipotropes methionine laurate myristate linolenate
Submitted on September 3, 1968
Copyright © 1969 by Lipid Research, Inc.
Fatty liver produced by dietary deficiencies: its pathogenesis and potentiation by ethanol
Accepted on January 20, 1969
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