Exogenous insulin does not influence CCK- and meal-stimulated pancreatic secretion

Although previous reports suggest interactions between the endocrine and the exocrine pancreas, insulin's effect on pancreatic exocrine function remains unclear, Chronic pancreatic fistulae were created in five dogs; these animals were studied using the euglycemic, hyperinsulinemic clamp technique. After a 30-min unstimulated period, both groups received a 60-min, 1.5 mU/kg/min insulin (clamp) or vehicle (control) infusion. Cholecystokinin (CCK) or meal stimulation was then begun. Intravenous CCK was initiated at 12.5 ng/kg/h; the CCK dose was doubled every 30 min until 100 ng/kg/h was achieved. The intraduodenal liquid test meal (1.5 kcal/ml; 15% protein, 32% fat, 53% carbohydrate) was administered at 100 ml/h. Unstimulated (0- to 30-min) serum glucose and insulin levels and pancreatic bicarbonate and protein outputs did not differ between groups. Clamp (30- to 90-min) and stimulated (90- to 210-min) insulins were significantly elevated in clamp groups (p < 0.001); glucose and bicarbonate were unchanged. Exocrine outputs during clamp periods were unaffected by insulin. Neither CCK- nor meal-stimulated pancreatic secretion (90-210 min) was influenced by insulin administration. These data suggest that hyperinsulinemia does not alter pancreatic acinar cell secretion in the intact animal.