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

Dig Dis Sci. 1996 Jul;41(7):1327-31. doi: 10.1007/BF02088555.


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.

MeSH terms

  • Adult
  • Blood Glucose / analysis
  • Eating*
  • Female
  • Gastrins / blood
  • Gastritis / blood*
  • Gastritis / microbiology
  • Glucose Tolerance Test
  • Helicobacter Infections / blood*
  • Helicobacter Infections / drug therapy
  • Helicobacter pylori*
  • Humans
  • Insulin / blood*
  • Male
  • Middle Aged


  • Blood Glucose
  • Gastrins
  • Insulin