The coupling of glucose metabolism and perfusion in human skeletal muscle - The potential role of endothelium-derived nitric oxide
The coupling of glucose metabolism and perfusion in human skeletal muscle - The potential role of endothelium-derived nitric oxide
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DOI：
10.2337/diab.45.1.s105
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发表时间：
1996-01-01
期刊：
影响因子：
7.7
通讯作者：
Baron, AD
中科院分区：
文献类型：
--
作者：
Baron, AD
骨骼肌中胰岛素介导的葡萄糖代谢与肌肉灌注的相应增加相关。胰岛素作用和血管舒张之间的联系可能是由内皮源性一氧化氮（EDNO）介导的。有证据表明，胰岛素引起胰岛素敏感但胰岛素抵抗受试者中EDNO产生的增加。胰岛素介导的血管舒张的这种缺陷可能导致1）升压敏感性增强和2）胰岛素介导的葡萄糖摄取速率降低。我们提出内皮是胰岛素靶组织，其表现出响应于胰岛素的EDNO释放增加。我们推测肥胖的胰岛素抵抗状态与内皮水平的胰岛素抵抗、EDNO释放减少和血管舒张受损相关，因此EDNO可能作为介导剂将葡萄糖代谢与血管舒张耦合。胰岛素和内皮细胞之间的相互作用，以增强EDNO的释放描述了一种新的胰岛素作用，值得进一步探索。
Insulin-mediated glucose metabolism in skeletal muscle is associated,vith a commensurate increase in muscle perfusion. The Link between insulin action and vasodilation may be mediated by endothelium-derived nitric oxide (EDNO). The evidence suggests that insulin causes an increase in the production of EDNO in insulin-sensitive but not insulin-resistant subjects. This defect in insulin-mediated vasodilation may contribute to 1) enhanced pressor sensitivity and 2) reduced rates of insulin-mediated glucose uptake, We propose that the endothelium is an insulin target tissue that exhibits an increase in the release of EDNO in response to insulin. We postulate that the insulin-resistant state of obesity is associated with insulin resistance at the level of the endothelium, reduced EDNO release, and impaired vasodilation, Thus EDNO may act as the mediator coupling glucose metabolism to vasodilation. The interaction between insulin and the endothelium to enhance EDNO release describes a novel insulin action that deserves further exploration.