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

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Abstract
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.