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Enhanced Insulin-Stimulated Activation of Phosphatidylinositol 3-Kinase in the Liver of High-Fat-Fed Rats

机译:胰岛素刺激的高脂饮食大鼠肝脏中磷脂酰肌醇3-激酶的激活。

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摘要

Insulin receptor substrate (IRS)-1 and IRS-2, which mediated phosphatidylinositol (PI) 3-kinase activation, play essential roles in insulin-induced translocation of GLUT4 and in glycogen synthesis. In this study, we Investigated the process of PI 3-kinase activation via Binding with IRS-1 and -2 in liver, muscle, and fat of High-fat-fed rats, a model of insulin-resistant diabetes. In the liver of high-fat-fed rats, insulin increased the PI 3-kinase regulatory subunit p85a and the PI 3-kinase activities associated with IRS-1 3.6- and 2.4-fold, and with IRS-2, 4.7- and 3.0-fold, respectively, compared with those in control rats.
机译:介导磷脂酰肌醇(PI)3激酶激活的胰岛素受体底物(IRS)-1和IRS-2在胰岛素诱导的GLUT4易位和糖原合成中起重要作用。在这项研究中,我们研究了高脂饮食大鼠(一种胰岛素抵抗性糖尿病的模型)在肝脏,肌肉和脂肪中通过与IRS-1和-2结合而激活PI 3-激酶的过程。在高脂饮食大鼠的肝脏中,胰岛素使PI 3激酶调节亚基p85a和PI 3激酶活性与IRS-1分别为3.6和2.4倍,与IRS-2、4.7和3.0有关。分别是对照组的两倍。

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