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Published on: January 31, 2022
Pioglitazone induced gastric acid secretion
Anand Rotte1, Andreas F Mack, Madhuri Bhandaru
1Department of Physiology, University of Tübingen, Tübingen, Germany.
Summary
Pioglitazone, a PPARgamma agonist, increases gastric acid secretion by upregulating SGK1 expression and KCNQ1 channels. This effect was not observed in mice lacking SGK1, confirming SGK1
Area of Science:
- Gastroenterology
- Molecular Endocrinology
- Pharmacology
Background:
- PPARgamma agonists like pioglitazone are used for diabetes and other conditions.
- These agonists may influence gastric acid secretion via SGK1 and KCNQ1 channels.
Purpose of the Study:
- To investigate if pioglitazone upregulates SGK1 protein in gastric glands.
- To determine pioglitazone's effect on gastric acid secretion and related channel expression.
Main Methods:
- Administered pioglitazone to wild-type and SGK1-deficient mice.
- Analyzed SGK1 expression via Western blotting.
- Measured acid secretion using BCECF-fluorescence and assessed channel abundance via immunohistochemistry.
Main Results:
- Pioglitazone significantly increased SGK1 expression in wild-type mice.
- Gastric acid secretion (DeltapH/min) increased ~3-fold in wild-type mice treated with pioglitazone, but not in SGK1-deficient mice.
- Pioglitazone enhanced KCNQ1 and H+/K+-ATPase protein in wild-type mice, an effect absent in SGK1-deficient mice.
Conclusions:
- Pioglitazone increases gastric acid secretion.
- This increase is partly mediated by SGK1 expression and subsequent KCNQ1 channel upregulation.
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