Influence of Helicobacter pylori on gastric secretion and gastrin release in normal Chinese subjects
Related Experiment Video
Updated: Aug 19, 2026

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes
Published on: July 5, 2024
Background:
Controversy exists concerning the influence of Helicobacter pylori on gastric secretion. Hyper-, normo- and hyposecretion of gastric acid in normal subjects with H pylori infection have been reported, although there is no such report for Chinese subjects. The goal of this study was to identify the effect of H pylori on gastric secretion in normal Chinese subjects.
Methods:
Twenty normal subjects with a normal upper gastrointestinal tract by endoscopy were recruited. H pylori status was assayed by a rapid urease test. Gastric secretion and gastrin release were also measured.
Results:
Among the subjects studied, nine were infected with H pylori. All enrolled subjects were males. Age and body weight were similar between both groups. No significant difference was found in basal acid output, maximal acid output, basal pepsin output or maximal pepsin output between the H pylori-positive group (median, 1.1 mmol/hour, 95% confidence interval 0.2-3.6 mmol/hour; 8.0, 3.0-18.3 mmol/hour; 0, -1.3-11.2 mmol/hour; and 4.1, -4.2-59.3 mmol/hour, respectively) and the H pylori-negative group (2.5, -1.3-11.3 mmol/hour; 12.2, 8.7-26.9 mmol/hour; 4.3, 1.8-13.5 mmol/hour; and 14.8, -5.7-73.0 mmol/hour, respectively). Serum basal gastrin and pepsinogen I concentration were 63.5, 50.0-78.6 pg/ml and 75.1, 50.6-89.8 ng/ml in the H pylori-positive group, and 65.9, 50.2-79.8 pg/ml and 79.1, 59.5-120.1 ng/ml in the H pylori-negative group (p > 0.05).
Conclusions:
H pylori plays no role in the gastric secretion and gastrin release in normal Chinese subjects.
More Related Videos
05:23Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
03:33Rapid Detection of Fecal Antigen of Helicobacter pylori Infection Based on Double Antibody Sandwich Detection Technology
Published on: May 23, 2025
Related Concept Videos
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Mucosal Barrier of the Stomach
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Peptic Ulcer
Gastritis II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology