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This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0295v1 199/3/343    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hills, C. Articles by Bland, R. Search for Related Content PubMed PubMed Citation Articles by Hills, C. Articles by Bland, R.

C Hills, Department of Infection, Immunity and Inflammation, Leicester Medical School, Leicester , United Kingdom
P Squires, Department of Biological Sciences, The University of Warwick, Warwick, United Kingdom
R Bland, Department of Biological Sciences, The University of Warwick, Coventry, United Kingdom

Correspondence: Rosemary Bland, Email: rosemary.bland{at}warwick.ac.uk

Abstract

Diabetes is associated with a number of side effects including retinopathy, neuropathy, nephropathy and hypertension. Recent evidence has shown that serum and glucocorticoid inducible kinase-1 (SGK1) is increased in models of diabetic nephropathy. Whilst 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 (ENaC). 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.