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首页> 外文期刊>Cell metabolism >Impaired insulin signaling in endothelial cells reduces insulin-induced glucose uptake by skeletal muscle.
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Impaired insulin signaling in endothelial cells reduces insulin-induced glucose uptake by skeletal muscle.

机译：内皮细胞中胰岛素信号的受损会减少骨骼肌对胰岛素的葡萄糖摄取。

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摘要

In obese patients with type 2 diabetes, insulin delivery to and insulin-dependent glucose uptake by skeletal muscle are delayed and impaired. The mechanisms underlying the delay and impairment are unclear. We demonstrate that impaired insulin signaling in endothelial cells, due to reduced Irs2 expression and insulin-induced eNOS phosphorylation, causes attenuation of insulin-induced capillary recruitment and insulin delivery, which in turn reduces glucose uptake by skeletal muscle. Moreover, restoration of insulin-induced eNOS phosphorylation in endothelial cells completely reverses the reduction in capillary recruitment and insulin delivery in tissue-specific knockout mice lacking Irs2 in endothelial cells and fed a high-fat diet. As a result, glucose uptake by skeletal muscle is restored in these mice. Taken together, our results show that insulin signaling in endothelial cells plays a pivotal role in the regulation of glucose uptake by skeletal muscle. Furthermore, improving endothelial insulin signaling may serve as a therapeutic strategy for ameliorating skeletal muscle insulin resistance.
机译：在患有2型糖尿病的肥胖患者中，骨骼肌的胰岛素输送和胰岛素依赖的葡萄糖摄取被延迟和受损。延迟和损害的潜在机制尚不清楚。我们证明，由于减少的Irs2表达和胰岛素诱导的eNOS磷酸化，内皮细胞中的胰岛素信号传导受损，导致胰岛素诱导的毛细血管募集和胰岛素传递的减弱，进而降低了骨骼肌对葡萄糖的吸收。此外，在内皮细胞中胰岛素诱导的eNOS磷酸化的恢复完全逆转了在内皮细胞中缺少Irs2并喂养高脂饮食的组织特异性敲除小鼠中毛细血管募集和胰岛素递送的减少。结果，在这些小鼠中恢复了骨骼肌对葡萄糖的摄取。两者合计，我们的结果表明，内皮细胞中的胰岛素信号传导在骨骼肌对葡萄糖摄取的调节中起关键作用。此外，改善内皮胰岛素信号传导可作为改善骨骼肌胰岛素抵抗的治疗策略。

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