The effect of glucose and insulin on vagally induced gastrin, bombesin-like immunoreactivity and somatostatin secretion from the perfused rat stomach.

Previous studies in the isolated perfused rat stomach have shown that elevated glucose and insulin concentrations modulate BLI and somatostatin release during arterially administered peptidergic stimuli. In the present study the effect of elevated levels of glucose or insulin was examined on vagally induced changes of gastrin, somatostatin and BLI secretion. The lumen of the stomach was perfused with saline pH 7 or pH 2. Vagal stimulation (5 Hz, 1 msec, 10V) increased gastrin and BLI secretion and inhibited somatostatin release. The increase of the perfusate glucose concentration from 100 mg/dl to 150 or 300 mg/dl or the addition of insulin (100 microU/ml) augmented vagally stimulated gastrin release at luminal pH 7 but not pH2. Vagally induced inhibition of somatostatin was attenuated by both concentrations of glucose at either luminal pH while insulin had no effect. BLI secretion was affected neither by elevated glucose nor by insulin. On the other hand, the noncholinergic component of vagally induced BLI secretion in the presence of atropine was augmented by insulin. These data demonstrate that glucose and insulin can modulate vagally activated gastric neuroendocrine functions which could be of relevance during the ingestion of carbohydrate containing meals.