Abstract
The development of an acute fatty liver in rats following the admistration of ethanol was associated with a normal intravascular removal rate of albumin-bound palmitic acid-l-C 14. When compared to isocaloric glucose-treated control rats, the ethanol group manifested a normal rate of incorporation of palmitate-l-C 14 into hepatic triglycerides prior to, and during, the development of a fatty liver. The release of triglyceride from liver, as determined by plasma triglyceride radioactivity following palmitate-l-C 14, was also unaltered. The hypertriglyceredemic response to Triton was also normal in acute ethanol-treated rats. Significant depression of hepatic triglyceride metabolism was observed in the ethanol group and is considered to be a contributing factor to the development of the acute ethanol-induced fatty liver.
Published Version
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