Previous studies have demonstrated mostly inhibitory effects of elevated plasma glucose levels on gastric exo- and endocrine as well as motor functions. Because increased plasma glucose levels reduce vagai activity via the central nervous system, it remains unclear if glucose exerts a direct effect on gastric functions. Therefore, our study was designed to determine the effect of acute changes in glucose concentrations on the release of gastrin and bombesin-like immunoreactivity (BLI) from the isolated perfused rat stomach. Acute elevations of pert usate glucose from 100 to 200 mg/dl or from 100 to 300 mg/dl augmented BLI secretion significantly without affecting gastrin release. During an acute decrease from 200 to 30 mg/dl, the secretion of both peptides remained unchanged. When ace-tylcholine was administered to stimulate BLI and gastrin secretion, the elevation of perfusate glucose to 200 mg/dl and the decrease to 30 mg/dl attenuated BLI secretion, whereas gastrin secretion remained unchanged compared with the control experiments at 100 mg/dl glucose. On the other hand, the perfusion of vasoactive intestinal peptide (VIP) and Leu-enkephalin had no effect on BLI and gastrin secretion during 100 mg/dl glucose perfusion, but both peptides elicited a significant stimulatory effect on BLI secretion during a perfusate glucose concentration of 200 mg/dl without affecting gastrin secretion. In conclusion, our study demonstrates first that an acute increase of glucose augments basal BLI secretion. Second, cholinergically induced BLI secretion is attenuated by hypo- and hyperglycemia. Third, hyperglycemia augments BLI secretion in response to the neuropeptides VIP and Leu-enkephalin. Fourth, basal and stimulated gastrin secretion remains unchanged during acute alterations of perfusate glucose levels. Because bombesin is considered to be a putative peptidergic neurotransmitter, the present data indicate that acute changes in glucose levels can affect neuronal activity, not only in the central nervous system, but also in the autonomie nervous system of the stomach. Our findings may be relevant in the study of disturbances of gastrointestinal functions in diabetes mellitus.

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