Hills Claire E, Squires Paul E, Bland Rosemary
Department of Biological Sciences, Biomedical Research Institute, The University of Warwick, Coventry CV4 7AL, UK.
J Endocrinol. 2008 Dec;199(3):343-9. doi: 10.1677/JOE-08-0295. Epub 2008 Jul 24.
Diabetes is associated with a number of side effects including retinopathy, neuropathy, nephropathy and hypertension. Recent evidence has shown that serum and glucocorticoid regulated kinase-1 (SGK1) is increased in models of diabetic nephropathy. While clearly identified as glucocorticoid responsive, SGK1 has also been shown to be acutely regulated by a variety of other factors. These include insulin, hypertonicity, glucose, increased intracellular calcium and transforming growth factor-beta, all of which have been shown to be increased in type II diabetes. The principal role of SGK1 is to mediate sodium reabsorption via its actions on the epithelial sodium channel (now known as sodium channel, nonvoltage-gated 1). Small alterations in the sodium resorptive capacity of the renal epithelia may have dramatic consequences for fluid volume regulation, and SGK1 maybe responsible for the development of hypertension associated with diabetes. This short commentary considers the evidence that supports the involvement of SGK1 in diabetic hypertension, but also discusses how aberrant sodium reabsorption may account for the cellular changes seen in the nephron.
糖尿病与多种副作用相关，包括视网膜病变、神经病变、肾病和高血压。最近的证据表明，在糖尿病肾病模型中，血清和糖皮质激素调节激酶-1（SGK1）水平升高。虽然SGK1被明确认为对糖皮质激素有反应，但它也已被证明受到多种其他因素的急性调节。这些因素包括胰岛素、高渗性、葡萄糖、细胞内钙增加和转化生长因子-β，所有这些在II型糖尿病中均已显示升高。SGK1的主要作用是通过其对上皮钠通道（现称为非电压门控钠通道1）的作用来介导钠重吸收。肾上皮细胞钠重吸收能力的微小改变可能对液体量调节产生巨大影响，并且SGK1可能是糖尿病相关高血压发生的原因。这篇简短的评论考虑了支持SGK1参与糖尿病性高血压的证据，但也讨论了异常的钠重吸收如何解释在肾单位中看到的细胞变化。
