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Studies on the Relationship between Lipogenesis and the Level of Coenzyme a Derivatives, Lactate and Pyruvate in Chick Liver¹

Laboratory of Nutritional Biochemistry, Department of Animal Science, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801

An attempt was made to elucidate the mechanisms by which hepatic lipogenesis is regulated by dietary protein and fat and by food restriction and refeeding in the growing chick. The reduction in hepatic fatty acid synthesis in fat-fed and short-term fasted chicks was accompanied by a decrease in the hepatic concentration of free CoA and in the lactate/pyruvate ratio and by an increase in the level of plasma free fatty acids and liver long-chain acyl-CoA derivatives. The data indicate that the depression in hepatic fatty acid synthesis caused by either fat feeding or short periods of fast can be attributed to: 1) a reduced availability of free CoA for citrate cleavage activity which would limit cytoplasmic acetyl-CoA generation for fatty acid synthesis; and 2) a decreased availability of cytoplasmic reducing equivalents to support reductive fatty acid biosynthesis. Increased dietary protein levels depressed hepatic lipogenesis and decreased plasma free fatty acid levels and the liver lactate/pyruvate ratio. Increased dietary protein did not, however, influence the hepatic levels of free CoA or acetyl-CoA in spite of the fact that long-chain acyl-CoA derivative levels were increased. The decreased ratio of lactate/pyruvate suggests that a limitation in the availability of cytoplasmic reducing equivalents may initiate the reduction in hepatic fatty acid synthesis in chicks fed high protein diets.

² Present address: Department of Chemistry, Utah State University, Logan, Utah 84321.

Manuscript received 22 January 1971.