Abstract

The mechanism of periportal fatty liver caused by dietary protein deficiency was investigated in the rhesus monkey by studying the pattern of Triton-induced hypertriglyceridemia. As compared with control animals fed an isocaloric high protein diet, the post-Triton hypertriglyceridemia was significantly less in the protein-deficient animals. This was reversed upon protein repletion in diet. Protein deficiency resulted in a reduction in plasma triglycerides and phospholipids, a rise in free fatty acids, and a fatty liver chiefly owing to accumulation of triglycerides associated with a reduction in hepatic phospholipids. It is concluded that the fatty liver of protein deficiency is predominantly due to a defect in the secretion of hepatic triglycerides.

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