Augmented gastric inhibitory polypeptide response to intraduodenal glucose by exogenous gastrin and cholecystokinin

Five awake dogs with Mann-Bollman fistulas each underwent six daily studies in which 50 ml of 20% glucose was infused intraduodenally (ID) over a period of 10 minutes. In five of six studies, either gastrin, pentagastrin, cholecystokinin, secretin, or glucagon was infused intravenously (IV) for 30 minutes before and 120 minutes after ID administered glucose. Venous blood samples at 15-minute intervals were assayed for immunoreactive gastric inhibitory peptide (GIP). IV administered gastrin, pentagastrin, cholecystokinin, secretin, and glucagon had no effect on fasting immunoreactive GIP (iGIP). Compared to fasting, iGIP was significantly (p < 0.05) increased at 15, 30, and 45 minutes for all treatment groups. Compared to ID administered glucose alone, the GIP response following either IV gastrin plus ID glucose, IV pentagastrin plus ID glucose, or IV cholecystokinin plus ID glucose was significantly greater (p < 0.05) at 5 and 15 minutes. This study demonstrates augmentation of glucose-stimulated GIP by the structurally similar peptides; gastrin, pentagastrin, and cholecystokinin, suggesting a physiological role for endogenous gastrin and cholecystokinin in modulating the GIP response to glucose.