Jones C T, Ashton I K
Biochem J. 1976 Jan 15;154(1):149-58. doi: 10.1042/bj1540149.
Lipid synthesis as measured by the incorporation of acetate or 3H2O into slices of foetal liver, is much higher than in slices of adult liver and shows a peak at about two-thirds of gestation. At this time the synthesis from glucose was low and reached a peak 10 days later. The changes in the activity of ATP citrate lyase, which mirrored acetate incorporation, and the effect of glucose and pyruvate on acetate corporation into lipid suggests that some of the lipid synthesis occurs via intramitochondrial acetyl-CoA production from acetate. Despite this, lipid synthesis was not inhibited by (-)-hydroxycitrate. The low rate of synthesis from glucose at two-thirds of gestation is ascribed to the low activity of pyruvate carboxylase at this time and a role for a phosphoenolpyruvate carboxykinase in providing oxaloacetate for lipogenesis is proposed. The activity of fatty acid synthetase broadly agreed with the changes in lipid synthesis, whereas the activity of acetyl-CoA carboxylase was barely sufficient to account for the rates of lipid synthesis in vivo. Acetate and short-chain fatty acids are likely to be the major precursors for lipid synthesis in vivo.
通过将乙酸盐或3H2O掺入胎儿肝脏切片来测定的脂质合成,比成年肝脏切片中的脂质合成要高得多,并且在妊娠约三分之二时达到峰值。此时,由葡萄糖进行的合成较低,并在10天后达到峰值。ATP柠檬酸裂解酶活性的变化反映了乙酸盐的掺入情况,以及葡萄糖和丙酮酸对乙酸盐掺入脂质的影响,这表明部分脂质合成是通过乙酸盐在线粒体内产生乙酰辅酶A来进行的。尽管如此,脂质合成并未被(-)-羟基柠檬酸抑制。妊娠三分之二时葡萄糖合成率较低,这归因于此时丙酮酸羧化酶的低活性,并提出磷酸烯醇式丙酮酸羧激酶在为脂肪生成提供草酰乙酸方面发挥作用。脂肪酸合成酶的活性与脂质合成的变化大致相符,而乙酰辅酶A羧化酶的活性几乎不足以解释体内脂质合成的速率。乙酸盐和短链脂肪酸可能是体内脂质合成的主要前体。