RESUMEN
Disturbances in gastric secretions are commonly associated with diabetes mellitus and are usually attributed to autonomic neuropathy. Systematic documentation of the effects of experimental diabetes on parietal cell functions are not available. This study has been designed to evaluate the acid secretory status of the parietal cells in streptozotocin (STZ) induced rat model of diabetes mellitus by assessing the effect of bilateral gastric vagotomy and histamine administration on them. Results show that bilateral gastric vagotomy in the control rats as well as in experimental diabetes lowers the acid secreting capacity of the parietal cells. In the diabetic rats, however, vagotomy does not further decrease the gastric acid secretion. Histamine stimulation augments the acid secretory response in the controls but this rise is substantially prevented in the diabetic state. Histamine challenge following vagotomy in normal controls elicits a sharp rise in gastric acid secretion though not to the same extent as seen in rats with intact vagi. In the diabetic rats however, histamine fails to augment acid secretion after vagotomy. Diabetes is thus seen to severely impair the acid secretory response of the parietal cells and their responsiveness to histamine.