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首页> 外文期刊>Diabetes >Insulin-Stimulated Phosphorylation of the Akt Substrate AS160 Is Impaired in Skeletal Muscle of Type 2 Diabetic Subjects.
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Insulin-Stimulated Phosphorylation of the Akt Substrate AS160 Is Impaired in Skeletal Muscle of Type 2 Diabetic Subjects.

机译：Akt底物AS160的胰岛素刺激的磷酸化在2型糖尿病患者的骨骼肌中受损。

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AS160 is a newly described substrate for the protein kinase Akt that links insulin signaling and GLUT4 trafficking. In this study, we determined the expression of and in vivo insulin action on AS160 in human skeletal muscle. In addition, we compared the effect of physiological hyperinsulinemia on AS160 phosphorylation in 10 lean-to-moderately obese type 2 diabetic and 9 healthy subjects. Insulin infusion increased the phosphorylation of several proteins reacting with a phospho-Akt substrate antibody. We focused on AS160, as this Akt substrate has been linked to glucose transport. A 160-kDa phosphorylated protein was identified as AS160 by immunoblot analysis with an AS160-specific antibody. Physiological hyperinsulinemia increased AS160 phosphorylation 2.9-fold in skeletal muscle of control subjects (P < 0.001). Insulin-stimulated AS160 phosphorylation was reduced 39% (P < 0.05) in type 2 diabetic patients. AS160 protein expression was similar in type 2 diabetic and control subjects. Impaired AS160 phosphorylation was related to aberrant Akt signaling; insulin action on Akt Ser(473) phosphorylation was not significantly reduced in type 2 diabetic compared with control subjects, whereas Thr(308) phosphorylation was impaired 51% (P < 0.05). In conclusion, physiological hyperinsulinemia increases AS160 phosphorylation in human skeletal muscle. Moreover, defects in insulin action on AS160 may impair GLUT4 trafficking in type 2 diabetes.
机译：AS160是一种新描述的蛋白激酶Akt的底物，它与胰岛素信号传导和GLUT4转运相关。在这项研究中，我们确定了人体骨骼肌中AS160的表达和体内胰岛素作用。此外，我们比较了10名瘦到中度肥胖的2型糖尿病和9名健康受试者的生理性高胰岛素血症对AS160磷酸化的影响。胰岛素输注增加了与磷酸化Akt底物抗体反应的几种蛋白质的磷酸化。我们将重点放在AS160上，因为该Akt底物已与葡萄糖转运相关。通过用AS160特异性抗体进行的免疫印迹分析，将160kDa的磷酸化蛋白鉴定为AS160。生理性高胰岛素血症使对照组受试者骨骼肌中AS160磷酸化增加2.9倍（P <0.001）。在2型糖尿病患者中，胰岛素刺激的AS160磷酸化降低了39％（P <0.05）。 AS160蛋白表达在2型糖尿病和对照组中相似。 AS160磷酸化受损与Akt信号异常有关。 2型糖尿病的胰岛素对Akt Ser（473）磷酸化的作用与对照组相比没有显着降低，而Thr（308）磷酸化受损51％（P <0.05）。总之，生理性高胰岛素血症会增加人骨骼肌中的AS160磷酸化。此外，胰岛素对AS160的作用缺陷可能会损害2型糖尿病的GLUT4转运。

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