Regulation of the oxidative NADP-enzyme tissue levels in Drosophila melanogaster. I. Modulation by dietary carbohydrate and lipid

Wild‐type third instar larvae of Drosophila melanogaster fed a casein‐sucrose synthetic diet supplemented with phosphatidylcholine (4 mg/ml) possessed 33% more tissue lipid and a modified fatty acid profile compared to larvae fed a fat free‐sucrose diet. The rates of lipid synthesis and pentose shunt activity were 2.1 and 2.2 times greater respectively in larvae fed the fat free‐sucrose diet than in fat‐sucrose fed animals. The tissue concentrations of acetyl‐CoA and acytl‐CoA were 80 and 61% higher respectively, CoA 49% lower, and the NADPH/NADP+ ratio greater in fat‐sucrose fed larvae than in larvae fed a fat free‐sucrose diet. Thus, larvae effectively utilized dietary lipid for lipid synthesis and as a supplementary energy source to carbohydrate. Larval oxidative NADP‐enzyme tissue levels were dependent upon the interaction of at least three regulatory systems. Dietary carbohydrate induced high tissue levels of glucose‐6‐phosphate dehydrogenase (EC 1.1.1.49) and 6‐phospho‐gluconate dehydrogenase (EC 1.1.1.43), ostensibly via a glycolytic derivative. High tissue levels of malic enzyme (EC 1.1.1.40) and NADP‐isocitrate dehydrogenase (EC 1.1.1.42) were induced by an acetate derivative postulated to be formed by the Krebs cycle. In contrast, a fatty acid derivative, presumably a product of β‐oxidation, repressed the tissue levels of all four oxidative NADP‐enzymes in larvae. A model of induction and repression regulatory systems that are dependent on regulatory gene products is proposed.