Effect of cholecystokinin, secretin, and gastric inhibitory polypeptide on insulin release from the isolated perfused rat pancreas

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Abstract
GIP (gastric inhibitory peptide, 1 ng/ml perfusate), infusions of CCK [cholecystokinin] stimulated significant insulin release both on a weight (1 ng/ml) and a molar (770 pg/ml) basis. Although 50% as potent as GIP on a weight basis and 43% as potent on a molar basis, the insulin response to CCK was multiphasic and sustained for the duration of the infusion. The action of CCK, like that of GIP, was glucose-dependent yielding no significant insulin release at a low perfusate glucose concentration (80 mg/dl). Irrespective of perfusate glucose concentration or dose (1 or 5 ng/ml), secretin failed to stimulate significant release of insulin from the perfused pancreas. Secretin is ineffective as an incretin. A physiological role for CCK in an enteroinsular axis awaits accurate measurement of circulating levels of immunoreactive CCK.