Interactions in vivo between oxidation of non-esterified fatty acids and gluconeogenesis in the newborn rat.
Interactions in vivo between oxidation of non-esterified fatty acids and gluconeogenesis in the newborn rat.
复制标题
新生大鼠体内非酯化脂肪酸氧化与糖异生之间的相互作用。
作者：
P. Ferré;J. Pégorier;D. Williamson;J. Girard
在不同营养状态下的 16 小时龄新生大鼠体内研究了脂肪酸氧化和糖异生之间的代谢相互作用。由于新生大鼠没有白色脂肪组织，出生后的饥饿会导致肝脏脂肪酸氧化率较低。与通过乳汁接收脂肪酸的乳鼠相比，在丙酮酸羧化酶和甘油醛3-磷酸脱氢酶催化的步骤中，饥饿的新生大鼠的肝糖异生受到抑制。这些抑制作用可通过三酰甘油喂养迅速逆转。哺乳动物中 pent-4-enoate 对脂肪酸氧化的抑制模拟了饥饿对肝糖异生代谢物模式的影响。结论是，在新生大鼠体内，肝脂肪酸氧化可以通过提供丙酮酸羧化酶催化反应所需的乙酰辅酶A和还原当量(NADH)来增加糖异生通量，以在糖异生方向上取代3-磷酸甘油醛脱氢酶催化的可逆反应。
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.