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2 型糖尿病中内皮胰岛素抵抗机制的新见解。

New insights into mechanisms of endothelial insulin resistance in type 2 diabetes.

机构信息

Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri.

NextGen Precision Health, University of Missouri, Columbia, Missouri.

出版信息

Am J Physiol Heart Circ Physiol. 2022 Dec 1;323(6):H1231-H1238. doi: 10.1152/ajpheart.00537.2022. Epub 2022 Nov 4.

Abstract

Insulin resistance in the vasculature is a hallmark of type 2 diabetes (T2D), and blunting of insulin-induced vasodilation is its primary consequence. Individuals with T2D exhibit a marked impairment in insulin-induced dilation in resistance arteries across vascular beds. Importantly, reduced insulin-stimulated vasodilation and blood flow to skeletal muscle limits glucose uptake and contributes to impaired glucose control in T2D. The study of mechanisms responsible for the suppressed vasodilatory effects of insulin has been a growing topic of interest for not only its association with glucose control and extension to T2D but also its relationship with cardiovascular disease development and progression. In this mini-review, we integrate findings from recent studies by our group with the existing literature focused on the mechanisms underlying endothelial insulin resistance in T2D.

摘要

血管胰岛素抵抗是 2 型糖尿病(T2D)的一个标志,而胰岛素诱导的血管舒张功能减弱是其主要后果。T2D 患者在血管床的阻力动脉中表现出明显的胰岛素诱导舒张功能障碍。重要的是,减少胰岛素刺激的血管舒张和血流到骨骼肌限制葡萄糖摄取,并导致 T2D 中的葡萄糖控制受损。研究导致胰岛素舒张作用受抑制的机制一直是一个日益受到关注的话题,不仅因为其与葡萄糖控制的关系以及对 T2D 的扩展,还因为其与心血管疾病的发展和进展的关系。在这个小型综述中,我们整合了我们小组最近的研究结果以及现有的文献,重点关注 T2D 中内皮胰岛素抵抗的机制。

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