Guzmán M, Castro J
Department of Biochemistry and Molecular Biology I, Faculty of Chemistry, Complutense University, Madrid, Spain.
Arch Biochem Biophys. 1990 Nov 15;283(1):90-5. doi: 10.1016/0003-9861(90)90616-7.
When added to the hepatocyte incubation medium, vanadate increased the rate of fatty acid synthesis de novo as well as the activity of acetyl-CoA carboxylase, whereas it had no effect on the activity of fatty acid synthase. On the other hand, and despite elevating the intracellular levels of malonyl-CoA, vanadate diverted exogenous fatty acids into the oxidation pathway at the expense of the esterification route. This was concomitant to an increase in carnitine palmitoyltransferase I activity. All these effects were not significantly different between periportal and perivenous hepatocytes and were also evident in cells incubated in Ca2(+)-free medium. Nevertheless, Ca2+ ions enhanced carnitine palmitoyltransferase I activity in isolated liver mitochondria. In addition, the effects of vanadate on acetyl-CoA carboxylase and carnitine palmitoyltransferase I were only evident in a permeabilized-cell assay, disappearing upon cell disruption and isolation of the corresponding cell subfraction for enzyme assay. Results show that vanadate exerts specific insulin-like and non-insulin-like effects on hepatic fatty acid metabolism, and suggest that the intracellular concentration of malonyl-CoA is not the only factor responsible for the regulation of the fatty-acid-oxidative process in the liver.
当添加到肝细胞孵育培养基中时，钒酸盐增加了从头脂肪酸合成的速率以及乙酰辅酶A羧化酶的活性，而对脂肪酸合酶的活性没有影响。另一方面，尽管钒酸盐提高了细胞内丙二酰辅酶A的水平，但它却将外源性脂肪酸导向氧化途径，而以酯化途径为代价。这伴随着肉碱棕榈酰转移酶I活性的增加。在门静脉周围和肝静脉周围的肝细胞之间，所有这些效应没有显著差异，并且在无Ca2+培养基中孵育的细胞中也很明显。然而，Ca2+离子增强了分离的肝线粒体中肉碱棕榈酰转移酶I的活性。此外，钒酸盐对乙酰辅酶A羧化酶和肉碱棕榈酰转移酶I的影响仅在透化细胞测定中明显，在细胞破碎并分离相应的细胞亚组分进行酶测定时消失。结果表明，钒酸盐对肝脏脂肪酸代谢发挥特定的胰岛素样和非胰岛素样作用，并表明细胞内丙二酰辅酶A的浓度不是肝脏中脂肪酸氧化过程调节的唯一负责因素。
