Ferré P, Pégorier J P, Williamson D H, Girard J
Biochem J. 1979 Aug 15;182(2):593-8. doi: 10.1042/bj1820593.
Metabolic interactions between fatty acid oxidation and gluconeogenesis were investigated in vivo in 16h-old newborn rats under various nutritional states. As the newborn rat has no white adipose tissue, starvation from birth induces a low rate of hepatic fatty acid oxidation. Hepatic gluconeogenesis in inhibited in the starved newborn rat when compared with the suckling rat, which receives fatty acids through the milk, at the steps catalysed by pyruvate carboxylase and glyceraldehyde 3-phosphate dehydrogenase. These inhibitions are rapidly reversed by triacylglycerol feeding. Inhibition of fatty acid oxidation by pent-4-enoate in the suckling animal mimics the effect of starvation on the pattern of hepatic gluconeogenic metabolites. It is concluded that, in the newborn rat in vivo, hepatic fatty acids oxidation can increase the gluconeogenic flux by providing the acetyl-CoA necessary for the reaction catalysed by pyruvate carboxylase and the reducing equivalents (NADH) to displace the reversible reaction catalysed by glyceraldehyde 3-phosphate dehydrogenase in the direction of gluconeogenesis.
在不同营养状态下,对16小时大的新生大鼠体内脂肪酸氧化与糖异生之间的代谢相互作用进行了研究。由于新生大鼠没有白色脂肪组织,出生后饥饿会导致肝脏脂肪酸氧化速率较低。与通过乳汁摄取脂肪酸的哺乳大鼠相比,饥饿的新生大鼠在丙酮酸羧化酶和甘油醛-3-磷酸脱氢酶催化的步骤中,肝脏糖异生受到抑制。通过喂食三酰甘油可迅速逆转这些抑制作用。在哺乳动物中,戊-4-烯酸对脂肪酸氧化的抑制作用模拟了饥饿对肝脏糖异生代谢物模式的影响。得出的结论是,在新生大鼠体内,肝脏脂肪酸氧化可通过提供丙酮酸羧化酶催化反应所需的乙酰辅酶A以及还原当量(NADH),来取代甘油醛-3-磷酸脱氢酶催化的可逆反应,使糖异生朝着生成葡萄糖的方向进行,从而增加糖异生通量。