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Tissue-specific regulation of early steps in insulin action in septic rats.

机译：脓毒症大鼠胰岛素作用早期步骤的组织特异性调节。

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Sepsis is known to induce insulin resistance, but the exact molecular mechanism involved is unknown. In the present study we have examined the levels and phosphorylation state of the insulin receptor and of insulin receptor substrate 1 (IRS-1), as well as the association between IRS-1 and phosphatidylinositol 3-kinase (PI 3-kinase) in the liver and muscle of septic rats by immunoprecipitation and immunoblotting with anti-insulin receptor, anti-IRS-1, anti-PI 3-kinase and anti-phosphotyrosine antibodies. There were no changes in the insulin receptor concentration and phosphorylation levels in the liver and muscle of septic rats. IRS-1 protein levels were decreased by 40+/-3% (p < 0.01) in muscle but not in liver of septic rats. In samples previously immunoprecipitated with anti-IRS-1 antibody and blotted with antiphosphotyrosine antibody, the insulin-stimulated IRS-1 phosphorylation levels in the muscle of septic rats decreased by 38+/-5% (p < 0.01) and insulin-stimulated IRS-1 association with PI 3-kinase decreased by 44+/-7% in muscle (p < 0.01) but no changes were seen in liver. These data suggest that there is a tissue-specific regulation of early steps of insulin signal transduction in septic rats, and the changes observed in muscle may have a role in the insulin resistance of these animals.
机译：已知败血症可诱导胰岛素抵抗，但尚不清楚确切的分子机制。在本研究中，我们检查了胰岛素受体和胰岛素受体底物1（IRS-1）的水平和磷酸化状态，以及IRS-1和磷脂酰肌醇3-激酶（PI 3-激酶）之间的关系。用抗胰岛素受体，抗IRS-1，抗PI 3-激酶和抗磷酸酪氨酸抗体进行免疫沉淀和免疫印迹，对败血症大鼠的肝脏和肌肉进行免疫沉淀。在脓毒症大鼠的肝脏和肌肉中，胰岛素受体的浓度和磷酸化水平没有变化。 IRS-1蛋白水平在脓毒症大鼠的肌肉中降低了40 +/- 3％（p <0.01），而在肝脏中没有降低。在先前用抗IRS-1抗体免疫沉淀并用抗磷酸酪氨酸抗体印迹的样品中，脓毒症大鼠肌肉中胰岛素刺激的IRS-1磷酸化水平降低了38 +/- 5％（p <0.01），胰岛素刺激的IRS降低了-1与PI 3-激酶的结合在肌肉中降低了44 +/- 7％（p <0.01），但在肝脏中未见变化。这些数据表明在脓毒症大鼠中胰岛素信号转导的早期步骤具有组织特异性调节，并且在肌肉中观察到的变化可能在这些动物的胰岛素抵抗中起作用。

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