The animal studies in mice found that gastrin, which stimulates the secretion of gastric acid, is an essential co-factor for Helicobacter-associated gastric carcinogenesis.
Dr. Timothy C. Wang from Columbia University Medical Center, New York, and colleagues say their research indicates that gastrin has a distinct effect on the gastric corpus and antrum in the setting of chronic Helicobacter infection.
In the study the team infected hypergastrinemic transgenic mice, gastrin knockout mice, and wild-type mice with Helicobacter felis.
At 18 months postinfection, hypergastrinemic mice and wild-type mice showed severe atrophic gastritis and corpus dysplasia, whereas gastrin-deficient mice had only severe gastritis with mild gastric atrophy but no corpus dysplasia.
On the other hand gastric knockout mice and wild-type mice had mild to moderate antral dysplasia at 18 months postinfection, but hypergastrinemic mice did not have progressive antral disease at this time point.
These results indicate that gastrin may have distinct effects on epithelial homeostasis between the gastric corpus and antrum, Dr. Wang and colleagues write.
The researchers concluded that the data are consistent with a model in which gastrin functions as a rheostat for the stomach.
Gastrin, they explain, plays a central role in the safety network for the protection from mucosal damages caused by gastric acid secretion induced by gastrin itself, and thus either too much or too little gastrin can predispose to carcinogenesis.