Effects of Cholecystokinin (CCK)-4, Nonsulfated CCK-8, and Sulfated CCK-8 on Pancreatic Somatostatin, Insulin, and Glucagon Secretion in the Dog: Studiesin Vitro*
Kjeld Hermansen
Abstract
Kjeld Hermansen
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, insulin, and glucagon release. The insulinotropic and glucagonotropic potency of CCK-8 was significantly greater than that of CCK-4, whereas the effect on SRIF secretion was similar. Furthermore, CCK-8-S and CCK-8 at concentrations of 0.1, 1, and 10 nM caused a dose-dependent increase in pancreatic A, B, and D cell secretion. The CCK-8-S was a more potent insulinotropic agent than CCK-8. It is suggested that these principal molecular CCK forms qualify for a physiological modulatory role in the endocrine pancreas.
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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, insulin, and glucagon release. The insulinotropic and glucagonotropic potency of CCK-8 was significantly greater than that of CCK-4, whereas the effect on SRIF secretion was similar. Furthermore, CCK-8-S and CCK-8 at concentrations of 0.1, 1, and 10 nM caused a dose-dependent increase in pancreatic A, B, and D cell secretion. The CCK-8-S was a more potent insulinotropic agent than CCK-8. It is suggested that these principal molecular CCK forms qualify for a physiological modulatory role in the endocrine pancreas.
Key concepts: Cholecystokinin, Internal medicine, Endocrinology, Somatostatin, Gastrointestinal hormone, Pancreas, Chemistry, Cholecystokinin receptor