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Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
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Related Experiment Video

Updated: Jun 25, 2026

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia

Published on: February 16, 2024

APC sensitive gastric acid secretion.

Anand Rotte¹, Madhuri Bhandaru, Michael Föller

¹Department of Physiology, University of Tubingen, Tubingen, Germany.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology

|March 4, 2009

Summary

This summary is machine-generated.

The tumor suppressor gene Adenomatous polyposis coli (APC) regulates gastric acid secretion. Loss of APC function in mice enhances gastric acid secretion, partly via SGK1-dependent KCNQ1 upregulation.

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Last Updated: Jun 25, 2026

Establishment and Evaluation of a Risk Prediction Model for Pathological Escalation of Gastric Low-Grade Intraepithelial Neoplasia

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Published on: February 16, 2024

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Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

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Published on: March 7, 2025

Area of Science:

Gastroenterology
Molecular Biology
Oncology

Background:

Adenomatous polyposis coli (APC) is a critical tumor suppressor gene implicated in colorectal cancer.
APC loss-of-function mutations lead to gastrointestinal tumor development in mice (apc(Min/+)).
APC influences beta-catenin degradation, impacting downstream signaling pathways.

Purpose of the Study:

To investigate the role of APC in regulating gastric acid secretion.
To elucidate the molecular mechanisms linking APC to gastric acid production.

Main Methods:

Gastric acid secretion measured using BCECF-fluorescence in isolated gastric glands.
Western blotting analyzed beta-catenin and SGK1 expression.
Immunohistochemistry assessed KCNQ1 protein levels.

Main Results:

apc(Min/+) mice exhibited enhanced beta-catenin and SGK1 expression.
Gastric acid secretion, reflected by Na+-independent pH recovery (DeltapH/min), was significantly faster in apc(Min/+) mice.
This enhanced secretion was dependent on H+/K+ ATPase activity and SGK1, with SGK1-dependent KCNQ1 upregulation playing a role.

Conclusions:

Basal gastric acid secretion is significantly enhanced in apc(Min/+) mice, indicating a regulatory role for APC.
The APC-mediated effect on gastric acid secretion involves H+/K+ ATPase activity.
SGK1-dependent upregulation of KCNQ1 is a key mechanism in this process.