J. Lipid Res.
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Journal of Lipid Research, Vol. 5, 437-441, July 1964
Copyright © 1964 by Lipid Research, Inc.

The role of liver and adipose tissue in the pathogenesis of the ethanol-induced fatty liver

Maria Poggi and N. R. Di Luzio

Department of Physiology, University of Tennessee Medical Units, Memphis, Tennessee

In vivo incubation of paired epididymal fat pads with medium containing palmitic acid-1-C14 was employed to label adipose tissue triglycerides. The administration of a single dose of ethanol to normal rats so treated produced an elevation of liver triglyceride, judged by comparison with control rats given glucose isocalorically. The radioactivity of liver triglyceride was proportionately elevated, while the specific activity was unchanged. The loss of radioactive triglyceride from adipose tissue was not significantly different in the ethanol group from that in the controls.

These studies demonstrate that adipose tissue triglyceride is mobilized at a normal rate during the development of this type of hepatic steatosis. Specific activity data suggest nevertheless that adipose tissue triglyceride fatty acids constitute the principal source of the fatty acids of the accumulated hepatic triglycerides, indicating an altered hepatic metabolism of triglycerides (or fatty acids) as the cause of the accumulation.

Submitted on July 18, 1963
Accepted on January 31, 1964


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G. O. Bustos, H. Kalant, J. M. Khanna, and J. Loth
Pyrazole and Induction of Fatty Liver by a Sigle Dose of Ethanol
Science, June 26, 1970; 168(3939): 1598 - 1599.
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