Geer B W, Langevin M L, McKechnie S W
Biochem Genet. 1985 Aug;23(7-8):607-22. doi: 10.1007/BF00504295.
When cultured on a defined diet, ethanol was an efficient substrate for lipid synthesis in wild-type Drosophila melanogaster larvae. At certain dietary levels both ethanol and sucrose could displace the other as a lipid substrate. In wild-type larvae more than 90% of the flux from ethanol to lipid was metabolized via the alcohol dehydrogenase (ADH) system. The ADH and aldehyde dehydrogenase activities of ADH were modulated in tandem by dietary ethanol, suggesting that ADH provided substrate for lipogenesis by degrading ethanol to acetaldehyde and then to acetic acid. The tissue activity of catalase was suppressed by dietary ethanol, implying that catalase was not a major factor in ethanol metabolism in larvae. The activities of lipogenic enzymes, sn-glycerol-3-phosphate dehydrogenase, fatty acid synthetase (FAS), and ADH, together with the triacylglycerol (TG) content of wild-type larvae increased in proportion to the dietary ethanol concentration to 4.5% (v/v). Dietary ethanol inhibited FAS and repressed the accumulation of TG in ADH-deficient larvae, suggesting that the levels of these factors may be subject to a complex feedback control.
当在限定饮食条件下培养时，乙醇是野生型黑腹果蝇幼虫脂质合成的有效底物。在特定饮食水平下，乙醇和蔗糖都可以相互替代作为脂质底物。在野生型幼虫中，超过90%从乙醇到脂质的通量是通过乙醇脱氢酶（ADH）系统代谢的。ADH的ADH和醛脱氢酶活性由饮食中的乙醇协同调节，这表明ADH通过将乙醇降解为乙醛然后再降解为乙酸为脂肪生成提供底物。饮食中的乙醇会抑制过氧化氢酶的组织活性，这意味着过氧化氢酶不是幼虫乙醇代谢的主要因素。野生型幼虫的脂肪生成酶、甘油-3-磷酸脱氢酶、脂肪酸合成酶（FAS）和ADH的活性，以及三酰甘油（TG）含量与饮食中乙醇浓度成比例增加，直至4.5%（v/v）。饮食中的乙醇抑制FAS并抑制ADH缺陷型幼虫中TG的积累，这表明这些因素的水平可能受到复杂的反馈控制。
