Does Helicobacter pylori-induced gastritis enhance food-stimulated insulin release?


Acbay Ö. , Celik A., Gundogdu S.

DIGESTIVE DISEASES AND SCIENCES, vol.41, pp.1327-1331, 1996 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 41
  • Publication Date: 1996
  • Doi Number: 10.1007/bf02088555
  • Title of Journal : DIGESTIVE DISEASES AND SCIENCES
  • Page Numbers: pp.1327-1331

Abstract

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.