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IRS1-independent defects define major nodes of insulin resistance.

机译：IRS1独立缺陷定义了胰岛素抵抗的主要节点。

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摘要

Insulin resistance is a common disorder caused by a wide variety of physiological insults, some of which include poor diet, inflammation, anti-inflammatory steroids, hyperinsulinemia, and dyslipidemia. The common link between these diverse insults and insulin resistance is widely considered to involve impaired insulin signaling, particularly at the level of the insulin receptor substrate (IRS). To test this model, we utilized a heterologous system involving the platelet-derived growth factor (PDGF) pathway that recapitulates many aspects of insulin action independently of IRS. We comprehensively analyzed six models of insulin resistance in three experimental systems and consistently observed defects in both insulin and PDGF action despite a range of insult-specific defects within the IRS-Akt nexus. These findings indicate that while insulin resistance is associated with multiple deficiencies, the most deleterious defects and the origin of insulin resistance occur independently of IRS.
机译：胰岛素抵抗是由多种生理损伤引起的常见疾病，其中一些饮食不良，炎症，抗炎类固醇，高胰岛素血症和血脂异常。这些多样的侮辱与胰岛素抵抗之间的共同联系被广泛认为涉及受损的胰岛素信号传导，尤其是在胰岛素受体底物（IRS）的水平上。为了测试该模型，我们利用了涉及血小板衍生生长因子（PDGF）途径的异源系统，该途径概括了独立于IRS的胰岛素作用的许多方面。我们在三个实验系统中全面分析了六种胰岛素抵抗模型，并且尽管在IRS-Akt内有一系列特定于损伤的缺陷，但始终观察到胰岛素和PDGF的作用均存在缺陷。这些发现表明，尽管胰岛素抵抗与多种缺陷有关，但最有害的缺陷和胰岛素抵抗的起源独立于IRS。

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