Abstract
The effect of cholecystokinin (CCK)-4, nonsulfated CCK-8 (CCK-8) and sulfated CCK-8 (CCK-8-S) on endocrine pancreas function was investigated in the isolated perfused dog pancreas in the presence of 5.5 mM glucose. CCK-4 and CCK-8 at concentrations of 1, 10 and 100 nM dose-dependently stimulated pancreatic SRIF [somatostatin], insulin and glucagon release. The insulinotropic and glucagonotropic potency of CCK-8 was significantly greater than that of CCK-4; the effect on SRIF secretion was similar. CCK-8-S and CCK-8 at concentrations of 0.1, 1 and 10 nM caused a dose-dependent increase in pancreatic A, .beta. and D cell secretion. The CCK-8-S was a more potent insulinotropic agent than CCK-8. Apparently, these principal molecular CCK forms qualify for a physiological modulatory role in the endocrine pancreas.

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