Hormonal Regulation of the Expression of the Genes for Malic Enzyme and Fatty Acid Synthase

In many cell types, the primary function of the pathway for de novo fatty acid synthesis is to provide long-chain fatty acids for membrane lipids. In the liver, however, the maximum rates of de novo fatty acid synthesis can be several orders of magnitude higher than that required for membrane biosynthesis. The primary function of hepatic lipogenesis is to convert excess dietary carbohydrate or protein to fatty acids, which are stored as triglyceride in adipose tissue and used as a source of energy during periods of restricted food intake. Regulation of hepatic fatty acid synthesis is consonant with this function. Thus, synthesis of long-chain fatty acids in the liver is inhibited by starvation, whereas refeeding starved animals stimulates fatty acid synthesis to normal levels or to supranormal levels if the diet is high in carbohydrate.(1,2)