Resistance to insulin and kidney disease in the cardiorenal metabolic syndrome; role for angiotensin II.

Resistance to insulin and kidney disease in the cardiorenal metabolic syndrome; role for angiotensin II.
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DOI:
10.1016/j.mce.2013.02.005
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发表时间:
2013-09-25
影响因子:
4.1
通讯作者:
Whaley-Connell, Adam
Whaley-Connell, Adam
中科院分区:
医学2区
文献类型:
--
作者:
Nistala, Ravi;Whaley-Connell, Adam

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胰岛素抵抗的存在越来越被认为是独立于糖尿病的早期肾脏疾病的重要贡献者。在这种关系中,重要的是高胰岛素血症和低水平白蛋白尿(例如微量白蛋白尿)之间的强相关性。最近的工作强调了过量胰岛素导致肾小球/肾小管间质损伤的机制,新出现的证据确定了胰岛素代谢信号传导的独特作用和近端小管水平盐重吸收的改变。也有证据表明胰岛素信号在肾小球上皮和内皮中的作用。损伤机制的核心是RAAS的不适当激活。
The presence of insulin resistance is increasingly recognized as an important contributor to early stage kidney disease independent of the contribution of diabetes. Important in this relationship is the strong correlation between hyperinsulinemia and low levels of albuminuria (e.g microalbuminuria). Recent work highlight mechanisms for glomerular/tubulointerstitial injury with excess insulin and emerging evidence identifies a unique role for insulin metabolic signaling and altered handling of salt reabsorption at the level of the proximal tubule. Evidence is also emerging for the role of insulin signaling in the glomerulus both epithelial and endothelial. Central to the mechanism of injury is inappropriate activation of the RAAS.
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