NDLI: Role of the serum and glucocorticoid inducible kinase SGK1 in glucocorticoid stimulation of gastric acid secretion

Content Provider	Springer Nature Link
Author	Sandu, Ciprian Artunc, Ferruh Grahammer, Florian Rotte, Anand Boini, Krishna M. Friedrich, Björn Sandulache, Diana Metzger, Marco Just, Lothar Mack, Andreas Skutella, Thomas Rexhepaj, Rexhep Risler, Teut Wulff, Peer Kuhl, Dietmar Lang, Florian
Copyright Year	2007
Abstract	Glucocorticoids stimulate gastric acid secretion, an effect favoring the development of peptic ulcers. Putative mechanisms involved include the serum- and glucocorticoid-inducible kinase (SGK1), which stimulates a variety of epithelial channels and transporters. The present study explored the contribution of SGK1 to effects of glucocorticoids on gastric acid secretion. In isolated gastric glands from gene-targeted mice lacking functional SGK1 (sgk1 −/−) and their wild-type littermates (sgk1 +/+), H+-secretion (ΔpH/min) was determined utilizing 2′,7′-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF)-fluorescence, SGK1 transcript levels by in situ hybdridization, and expression of KCNQ1 channels by immunohistochemistry and real-time polymerase chain reaction. SGK1 transcript levels were enhanced by a 4-day treatment with 10 μg/g body weight (BW)/day dexamethasone (DEX). Before treatment, ΔpH/min was similar in sgk1 −/− and sgk1 +/+mice. DEX increased ΔpH/min ∼fourfold in sgk1 +/+mice and ∼twofold in sgk1 −/−mice, effects abolished in the presence of K+/H+ATPase-inhibitor omeprazole (50 μM). Increase in local K+ concentrations to 35 mM (replacing Na+) enhanced ΔpH/min, which could not be further stimulated by DEX and was not significantly different between sgk1 −/− and sgk1 +/+mice. Carbachol (100 μM) and forskolin (5 μM) stimulated gastric acid secretion to a similar extent in sgk1 −/− and sgk1 +/+mice. In conclusion, SGK1 is not required for basal and cyclic AMP-stimulated gastric H+ secretion but participates in the stimulation of gastric H+ secretion by glucocorticoids. The effects of glucocorticoids and SGK1 are not additive to an increase in extracellular K+ concentration and may thus involve stimulation of K+ channels.
Starting Page	493
Ending Page	503
Page Count	11
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	455
Issue Number	3
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	2007-07-06
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Glucocorticoids H+ secretion Stomach K+ channels Human Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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