The fact thatH. 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 whetherH. 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 withH. pylori gastritis before and one month after the eradication therapy and also in 15H. pylori-negative control subjects. The areas under the curve (AUC) for serum insulin following both oral glucose and a mixed meal in the patients withH. pylori gastritis before the eradication were significantly (P<0.05) higher="" than="" those="" in="">H. pylori-negative controls. After the eradication ofH. 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="">H. pylori gastritis enhances glucose and meal-stimulated insulin release probably by increasing gastrin secretion.