Decaux J F, Robin D, Robin P, Ferré P, Girard J
Centre de Recherches sur la Nutrition du CNRS, Meudon-Bellevue, France.
FEBS Lett. 1988 May 9;232(1):156-8. doi: 10.1016/0014-5793(88)80407-1.
Fatty acid oxidation was studied in isolated liver mitochondria of rats during the suckling-weaning transition. The oxidation rate of oleyl-CoA and palmitoylcarnitine was reduced 2.5-fold in rats weaned on a high-carbohydrate diet compared to suckling rats, when acetyl-CoA produced by beta-oxidation was directed towards ketone-body synthesis. Weaning on a high-fat diet minimized this change. Channeling of acetyl-CoA towards citrate synthesis doubled the oxidation rate of both substrates in HC-weaned rats. Thus, in addition to changes in carnitine palmitoyltransferase I activity, the beta-hydroxymethylglutaryl-CoA synthase pathway is also involved in the decreased fatty acid oxidation at weaning. This was confirmed by measurement of beta-hydroxymethylglutaryl-CoA synthase pathway activity.
在哺乳-断奶过渡期，对大鼠分离的肝脏线粒体中的脂肪酸氧化进行了研究。与哺乳大鼠相比，以高碳水化合物饮食断奶的大鼠中，油酰辅酶A和棕榈酰肉碱的氧化速率降低了2.5倍，此时β-氧化产生的乙酰辅酶A用于酮体合成。以高脂肪饮食断奶可使这种变化最小化。在高碳水化合物饮食断奶的大鼠中，乙酰辅酶A导向柠檬酸合成使两种底物的氧化速率加倍。因此，除了肉碱棕榈酰转移酶I活性的变化外，β-羟甲基戊二酰辅酶A合酶途径也参与了断奶时脂肪酸氧化的降低。通过测量β-羟甲基戊二酰辅酶A合酶途径的活性证实了这一点。
