Research ExplorerPublicationsPioglitazone induced gastric acid secretion.

Pioglitazone induced gastric acid secretion.

Standard

Pioglitazone induced gastric acid secretion. / Rotte, Anand; Mack, Andreas F; Bhandaru, Madhuri; Kempe, Daniela S; Beier, Norbert; Scholz, Wolfgang; Dicks, Edith; Pötzsch, Sven; Kuhl, Dietmar; Lang, Florian.

In: CELL PHYSIOL BIOCHEM, Vol. 24, No. 3-4, 3-4, 2009, p. 193-200.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Rotte, A, Mack, AF, Bhandaru, M, Kempe, DS, Beier, N, Scholz, W, Dicks, E, Pötzsch, S, Kuhl, D & Lang, F 2009, 'Pioglitazone induced gastric acid secretion.', CELL PHYSIOL BIOCHEM, vol. 24, no. 3-4, 3-4, pp. 193-200. https://doi.org/10.1159/000233245

APA

Rotte, A., Mack, A. F., Bhandaru, M., Kempe, D. S., Beier, N., Scholz, W., Dicks, E., Pötzsch, S., Kuhl, D., & Lang, F. (2009). Pioglitazone induced gastric acid secretion. CELL PHYSIOL BIOCHEM, 24(3-4), 193-200. [3-4]. https://doi.org/10.1159/000233245

Vancouver

Rotte A, Mack AF, Bhandaru M, Kempe DS, Beier N, Scholz W et al. Pioglitazone induced gastric acid secretion. CELL PHYSIOL BIOCHEM. 2009;24(3-4):193-200. 3-4. https://doi.org/10.1159/000233245

Bibtex

@article{eba8d859fc2445939afafb56f0b34ace,
title = "Pioglitazone induced gastric acid secretion.",
abstract = "PPARgamma agonists, such as pioglitazone, are widely used in the treatment of diabetes and several further disorders. They enhance transcription of the serum and glucocorticoid inducible kinase SGK1, which could in turn enhance gastric acid secretion by stimulating KCNQ1 K+ channels. The present study explored whether pioglitazone upregulates SGK1 protein expression in gastric glands and thus modifies gastric acid secretion. Food containing the PPARgamma agonist pioglitazone (approximately 25 mg/kg bw/day) was administered to gene-targeted mice lacking SGK1 (sgk1-/-, n=11) and their wild-type littermates (sgk1+/+, n=11). Western blotting was employed to analyze SGK1 expression, BCECF-fluorescence to determine acid secretion in isolated gastric glands and immunohistochemistry to elucidate KCNQ1 and H+/K+-ATPase protein abundance in the parietal cell membrane. Pioglitazone significantly increased SGK1 expression. Cytosolic pH and cellular buffer capacity were not significantly different between sgk1+/+ and sgk1-/- mice and not significantly modified in either genotype by pioglitazone. Without pioglitazone treatment, Na+-independent pH-recovery following an ammonium pulse (DeltapH/min) reflecting H+/K+-ATPase activity was again similar in sgk1+/+ and sgk1-/- mice. Pioglitazone significantly increased DeltapH/min (approximately 3 fold) in sgk1+/+ but not in sgk1-/- mice. H+/K+-ATPase inhibitor omeprazole (100 microM) abolished DeltapH/min in both genotypes irrespective of pioglitazone treatment. Increase in local K+ concentrations to 35 mM (replacing Na+/NMDG) significantly increased DeltapH/min and abrogated the differences between genotypes. KCNQ1 and H+/K+-ATPase protein abundance in the parietal cell membrane was enhanced by pioglitazone treatment in sgk1+/+ but not in sgk1-/- mice. In conclusion, pioglitazone increases gastric acid secretion, an effect at least partially due to stimulation of SGK1 expression and SGK1-dependent upregulation of KCNQ1.",
author = "Anand Rotte and Mack, {Andreas F} and Madhuri Bhandaru and Kempe, {Daniela S} and Norbert Beier and Wolfgang Scholz and Edith Dicks and Sven P{\"o}tzsch and Dietmar Kuhl and Florian Lang",
year = "2009",
doi = "10.1159/000233245",
language = "Deutsch",
volume = "24",
pages = "193--200",
journal = "CELL PHYSIOL BIOCHEM",
issn = "1015-8987",
publisher = "S. Karger AG",
number = "3-4",

}

RIS

TY - JOUR

T1 - Pioglitazone induced gastric acid secretion.

AU - Rotte, Anand

AU - Mack, Andreas F

AU - Bhandaru, Madhuri

AU - Kempe, Daniela S

AU - Beier, Norbert

AU - Scholz, Wolfgang

AU - Dicks, Edith

AU - Pötzsch, Sven

AU - Kuhl, Dietmar

AU - Lang, Florian

PY - 2009

Y1 - 2009

N2 - PPARgamma agonists, such as pioglitazone, are widely used in the treatment of diabetes and several further disorders. They enhance transcription of the serum and glucocorticoid inducible kinase SGK1, which could in turn enhance gastric acid secretion by stimulating KCNQ1 K+ channels. The present study explored whether pioglitazone upregulates SGK1 protein expression in gastric glands and thus modifies gastric acid secretion. Food containing the PPARgamma agonist pioglitazone (approximately 25 mg/kg bw/day) was administered to gene-targeted mice lacking SGK1 (sgk1-/-, n=11) and their wild-type littermates (sgk1+/+, n=11). Western blotting was employed to analyze SGK1 expression, BCECF-fluorescence to determine acid secretion in isolated gastric glands and immunohistochemistry to elucidate KCNQ1 and H+/K+-ATPase protein abundance in the parietal cell membrane. Pioglitazone significantly increased SGK1 expression. Cytosolic pH and cellular buffer capacity were not significantly different between sgk1+/+ and sgk1-/- mice and not significantly modified in either genotype by pioglitazone. Without pioglitazone treatment, Na+-independent pH-recovery following an ammonium pulse (DeltapH/min) reflecting H+/K+-ATPase activity was again similar in sgk1+/+ and sgk1-/- mice. Pioglitazone significantly increased DeltapH/min (approximately 3 fold) in sgk1+/+ but not in sgk1-/- mice. H+/K+-ATPase inhibitor omeprazole (100 microM) abolished DeltapH/min in both genotypes irrespective of pioglitazone treatment. Increase in local K+ concentrations to 35 mM (replacing Na+/NMDG) significantly increased DeltapH/min and abrogated the differences between genotypes. KCNQ1 and H+/K+-ATPase protein abundance in the parietal cell membrane was enhanced by pioglitazone treatment in sgk1+/+ but not in sgk1-/- mice. In conclusion, pioglitazone increases gastric acid secretion, an effect at least partially due to stimulation of SGK1 expression and SGK1-dependent upregulation of KCNQ1.

AB - PPARgamma agonists, such as pioglitazone, are widely used in the treatment of diabetes and several further disorders. They enhance transcription of the serum and glucocorticoid inducible kinase SGK1, which could in turn enhance gastric acid secretion by stimulating KCNQ1 K+ channels. The present study explored whether pioglitazone upregulates SGK1 protein expression in gastric glands and thus modifies gastric acid secretion. Food containing the PPARgamma agonist pioglitazone (approximately 25 mg/kg bw/day) was administered to gene-targeted mice lacking SGK1 (sgk1-/-, n=11) and their wild-type littermates (sgk1+/+, n=11). Western blotting was employed to analyze SGK1 expression, BCECF-fluorescence to determine acid secretion in isolated gastric glands and immunohistochemistry to elucidate KCNQ1 and H+/K+-ATPase protein abundance in the parietal cell membrane. Pioglitazone significantly increased SGK1 expression. Cytosolic pH and cellular buffer capacity were not significantly different between sgk1+/+ and sgk1-/- mice and not significantly modified in either genotype by pioglitazone. Without pioglitazone treatment, Na+-independent pH-recovery following an ammonium pulse (DeltapH/min) reflecting H+/K+-ATPase activity was again similar in sgk1+/+ and sgk1-/- mice. Pioglitazone significantly increased DeltapH/min (approximately 3 fold) in sgk1+/+ but not in sgk1-/- mice. H+/K+-ATPase inhibitor omeprazole (100 microM) abolished DeltapH/min in both genotypes irrespective of pioglitazone treatment. Increase in local K+ concentrations to 35 mM (replacing Na+/NMDG) significantly increased DeltapH/min and abrogated the differences between genotypes. KCNQ1 and H+/K+-ATPase protein abundance in the parietal cell membrane was enhanced by pioglitazone treatment in sgk1+/+ but not in sgk1-/- mice. In conclusion, pioglitazone increases gastric acid secretion, an effect at least partially due to stimulation of SGK1 expression and SGK1-dependent upregulation of KCNQ1.

U2 - 10.1159/000233245

DO - 10.1159/000233245

M3 - SCORING: Zeitschriftenaufsatz

VL - 24

SP - 193

EP - 200

JO - CELL PHYSIOL BIOCHEM

JF - CELL PHYSIOL BIOCHEM

SN - 1015-8987

IS - 3-4

M1 - 3-4

ER -