Hills, Claire E., Squires, Paul E. and Bland, Rosemary. (2008) SGK and disturbed renal sodium transport in diabetes. Journal of Endocrinology, Vol.199 (No.3). pp. 343-349. ISSN 0022-0795

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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.

Item Type:	Journal Article
Subjects:	R Medicine > RC Internal medicine
Divisions:	Faculty of Science > Life Sciences (2010- ) > Biological Sciences ( -2010)
Library of Congress Subject Headings (LCSH):	Diabetes -- Research, Kidneys -- Diseases, Diabetic nephropathies
Journal or Publication Title:	Journal of Endocrinology
Publisher:	Society for Endocrinology
ISSN:	0022-0795
Date:	2008
Volume:	Vol.199
Number:	No.3
Page Range:	pp. 343-349
Identification Number:	10.1677/JOE-08-0295
Status:	Peer Reviewed
Access rights to Published version:	Restricted or Subscription Access
Funder:	Diabetes, Endocrine and Immersion Research Trust, Diabetes UK
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URI:	http://wrap.warwick.ac.uk/id/eprint/383

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