Does Helicobacter pylori-induced gastritis enhance food-stimulated insulin release?
The fact that H. pylori gastritis results in an increased secretion of basal and meal-stimulated gastrin, which is also a physiologic amplifier of insulin release directed us to investigate whether H. pylori gastritis may lead to an enhancement of nutrient-stimulated insulin secretion. For this purpose, we have investigated the insulin responses to both oral glucose and a mixed meal in 15 patients with H. pylori gastritis before and one month after the eradication therapy and also in 15 H. pylori-negative control subjects. The areas under the curve (AUC) for serum insulin following both oral glucose and a mixed meal in the patients with H. pylori gastritis before the eradication were significantly (P < 0.05) higher than those in the H. pylori-negative controls. After the eradication of H. pylori, the AUC for serum insulin following oral glucose and mixed meal decreased by 9.4% and 13.1%, respectively (P < 0.001 in both), and serum basal and meal-stimulated gastrin levels decreased significantly (P < 0.001). These results suggest that H. pylori gastritis enhances glucose and meal-stimulated insulin release probably by increasing gastrin secretion.
Açbay
O
O
Department of Internal Medicine, Medical School Hospital, University of Istanbul, Turkey.
Celik
A F
AF
Gündoğdu
S
S
D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D004435:Eating; D005260:Female; D005755:Gastrins / Q000097:blood; D005756:Gastritis / Q000097:blood* / Q000382:microbiology; D005951:Glucose Tolerance Test; D016481:Helicobacter Infections / Q000097:blood* / Q000188:drug therapy; D016480:Helicobacter pylori; D006801:Humans; D007328:Insulin / Q000097:blood*; D008297:Male; D008875:Middle Aged
D001786:Blood Glucose; D005755:Gastrins; D007328:Insulin