The effect of bombesin on basal and glucose-stimulated insulin release was studied in male healthy volunteers. Glucose was administered by oral, intravenous or intraduodenal route during saline or bombesin infusion (5 ng/kg/min for 60 min). The peptide had no significant effect on basal levels of glucose and insulin. However, during its administration, the insulin response and the expected rise in blood glucose after oral glucose load (50 g) were strongly inhibited, and the gastric emptying of liquids was significantly delayed. On the contrary, the insulin response to intravenous glucose (20 g) was significantly increased by bombesin without changes in plasma glucose levels. Finally, when glucose was infused into the duodenum, thus bypassing the stomach, the insulin response was significantly increased by the peptide. In this case, too, plasma glucose levels after glucose load were virtually identical during either bombesin or saline infusion. These data clearly demonstrate that the direct effect of bombesin on insulin release is stimulatory and suggest that the inhibitory effect observed after oral glucose is connected with the action of the peptide on gastric emptying, the delay of which slows the entry of glucose into the small bowel.
The effect of bombesin, a neurograstrointestinal peptide, on basal and stimulated insulin release was studied in man. Two different stimuli were used, hyperglycaemic (20 g glucose) and hypoglycaemic (1 g tolbutamide). They were injected intravenously to two groups of male healthy volunteers during saline or bombesin (5 ng kg−1 min−1 for 60 min) infusion. The peptide had no significant effect on basal levels of glucose and insulin. However, the insulin response to intravenous glucose was strongly potentiated by bombesin, the integrated insulin response being 2.23 ± 0.59 mu ml−1 · 90 min and 0.98 ± 0.19 mu ml−1 · 90 min during infusion of bombesin and saline, respectively (P < 0.05). The behaviour of plasma glucose was not significantly modified by the peptide. Indeed, the glucose disappearance rate (K of Conard, mg min 10−2) changed from 2.5 ± 0.3 during saline to 2.4 ± 0.4 during bombesin infusion. When the hypoglycaemic stimulus (i.e. tolbutamide) was used, no effect of the peptide on insulin release could be detected. Here again, the drop in plasma glucose (expressed as Marigo's coefficient) was not affected by the peptide, with a value of 92.8 ± 12.6 and 84.0 ± 10.9 during bombesin and saline administration. These data therefore show that, at normal or low blood glucose levels, the dose of bombesin used is unable to modify insulin release and suggest that this peptide might be regarded as a glucose‐dependent insulinotropic peptide.
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