Alterations in duodenal bicarbonate secretion and mucosal susceptibility to acid in diabetic rats.

Abstract

The gastroduodenal mucosal susceptibility to ulcerogenic stimuli increases in diabetic conditions, but the mechanism is unknown. The aim of this study was to investigate alterations in duodenal HCO3- secretory response in diabetic animals. The experiments were performed in rats treated with streptozotocin (70 mg/kg intraperitoneally) after 1-6 weeks of diabetes, when blood glucose levels were > 300 mg/dL. HCO3 secretion was measured in the proximal duodenal loop of rats that were under urethane anesthesia using a pH-stat method. The duodenal HCO3 secretion induced by mucosal acidification was decreased in streptozotocin-treated rats depending on the duration of diabetes. The HCO3 secretion was also decreased in response to 16,16-dimethyl prostaglandin E2, vasoactive intestinal polypeptide, or vagal electrical stimulation. Acid load in the duodenum produced extensive damage in 5-6-week diabetic rats, although the same treatment caused only slight damage in the normal rat duodenum. Such alterations in the duodenal HCO3 secretory and ulcerogenic responses in diabetic rats were partially restored by daily injection of insulin. The results suggest that streptozotocin-diabetic conditions impair the duodenal HCO3- secretion in rats, possibly as a result of decreased sensitivity of the epithelial cell and dysfunction of neuronal pathway, thereby increasing the mucosal susceptibility to acid injury in the duodenum.