Açbay O, Celik A F, Gündoğdu S
Department of Internal Medicine, Medical School Hospital, University of Istanbul, Turkey.
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.
幽门螺杆菌胃炎会导致基础胃酸和餐食刺激后的胃泌素分泌增加，而胃泌素也是胰岛素释放的生理放大器，这一事实促使我们研究幽门螺杆菌胃炎是否可能导致营养物质刺激的胰岛素分泌增强。为此，我们调查了15例幽门螺杆菌胃炎患者在根除治疗前和治疗后1个月以及15例幽门螺杆菌阴性对照受试者对口服葡萄糖和混合餐的胰岛素反应。根除治疗前，幽门螺杆菌胃炎患者口服葡萄糖和混合餐后血清胰岛素的曲线下面积（AUC）显著高于（P < 0.05）幽门螺杆菌阴性对照受试者。根除幽门螺杆菌后，口服葡萄糖和混合餐后血清胰岛素的AUC分别下降了9.4%和13.1%（两者均P < 0.001），血清基础胃酸和餐食刺激后的胃泌素水平显著下降（P < 0.001）。这些结果表明，幽门螺杆菌胃炎可能通过增加胃泌素分泌来增强葡萄糖和餐食刺激的胰岛素释放。
