Levy J, Avioli L V, Roberts M L, Gavin J R
Biochem Biophys Res Commun. 1986 Sep 30;139(3):1313-9. doi: 10.1016/s0006-291x(86)80321-7.
Insulin resistant, Type II diabetes mellitus (NIDD) in a rat animal model results in profound changes in basal and insulin-stimulated membrane (Ca2+ +Mg2+)-ATPase activity in kidney basolateral membrane (BLM) preparations. We find that NIDD in these animals does not result in similar changes in membrane (Na+ +K+)-ATPase activity. Basal enzyme activity was the same in diabetic and control animals. Insulin treatment of diabetic animals in vivo resulted in hyperinsulinemia and increased BLM (Na+ +K+)-ATPase, while food restriction for 18 hr resulted in lowered enzyme activity. There was no direct effect of insulin on (Na+ +K+)-ATPase activity in isolated membranes from any of the animal groups. Thus, physiologic perturbations which alter insulin sensitivity and glucose homeostasis are accompanied by altered levels of (Na+ +K+)-ATPase activity. Lower levels of this membrane enzyme activity appear to be associated with optimal insulin action.
在大鼠动物模型中，胰岛素抵抗的II型糖尿病（NIDD）会导致肾基底外侧膜（BLM）制剂中基础和胰岛素刺激的膜（Ca2+ +Mg2+）-ATP酶活性发生深刻变化。我们发现，这些动物的NIDD不会导致膜（Na+ +K+）-ATP酶活性发生类似变化。糖尿病动物和对照动物的基础酶活性相同。对糖尿病动物进行体内胰岛素治疗会导致高胰岛素血症，并增加BLM（Na+ +K+）-ATP酶活性，而禁食18小时会导致酶活性降低。胰岛素对任何动物组的分离膜中的（Na+ +K+）-ATP酶活性均无直接影响。因此，改变胰岛素敏感性和葡萄糖稳态的生理扰动会伴随着（Na+ +K+）-ATP酶活性水平的改变。这种膜酶活性水平较低似乎与最佳胰岛素作用相关。
