Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2006; Volume 186, Supplement 650
Joint Meeting of The German Society of Physiology and The Federation of European Physiological Societies 2006
3/26/2006-3/29/2006
Ludwig-Maximilians-University, Munich


SGK1 DEPENDENT UPREGULATION OF INTESTINAL SGLT1 AND NHE3 BY DEXAMETHASONE
Abstract number: PW03P-12

Hussain1 A, Grahammer1 F, Henke1 G, Sandu1 C, Rexhepaj1 R, Artunc1 F, Friedrich1 B, Wulff1 P, Kuhl1 D, Lang1 F

1Eberhard-Karls-University of Tuebingen, Dept. of Physiology

Serum and glucocorticoid inducible kinase (SGK)1 is under the genomic control of several hormones including glucocorticoids. In vitro evidence suggests that SGK1 plays an important role in the modulation of several ion channels and transporters. In Xenopus laevis oocytes, it has been shown that the kinase modulates Na+, glucose cotransporter SGLT1 and Na+/H+ exchanger, NHE3 transporters. The present experiments have been performed to explore the role of SGK1 in modulating intestinal surface expression of SGLT1 and NHE3 in vivo. Specifically, the study aimed to analyse the influence of dexamethasone on expression of SGLT1 and NHE3, in intestine obtained from SGK1 wild type mice (sgk1+/+) and SGK1 knockout mice (sgk1-/-). According to western blotting, SGLT1 and NHE3 protein levels were similar in untreated wild type and knockout mice, but dexamethasone (10 mg/g BW/day) treatment led to a significant increase of SGLT1 and NHE3 expression in small intestine from sgk1+/+ mice but not in sgk1-/- mice. Moreover, increased SGLT1 plasma membrane expression was followed by an increase in carrier protein glycosylation. In conclusion, basal expression of SGLT1 and NHE3 in intestine does not require SGK1. However, the full effects of dexamethasone on SGLT1 and NHE3 protein expression and function are dependent on the kinase.

To cite this abstract, please use the following information:
Acta Physiologica 2006; Volume 186, Supplement 650 :PW03P-12

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE