Potentiation of cholecystokinin-induced exocrine secretion by both exogenous and endogenous insulin in isolated and perfused rat pancreata.
Using an isolated perfused rat pancreas preparation, the interrelationship between the endocrine and exocrine portions of the pancreas were studied. Addition of exogenous rat insulin (1-20 mU/ml) to the perfusing solution potentiated the action of cholecystokinin (CCK) (1 mU/ml) to increase both pancreatic juice flow and the release of the enzyme, amylase. Raising the glucose concentration in the perfusing solution from 2.5 to 17.5 mM both increased endogenous insulin release and potentiated the CCK-induced exocrine secretory response. Two lines of evidence indicated that this effect of glucose on the exocrine pancreas was mediated by endogenous insulin release. First, the addition of comparable amounts of xylose or galactose to the perfusion medium neither released insulin nor potentiated the CCK-induced response. Second, epinephrine blocked the effect of high glucose on both insulin release and potentiation of CCK action. Epinephrine alone did not affect the action of CCK. The magnitude of the exocrine response induced by high glucose was comparable to that of 2.5 mU/ml exogenous insulin. It seems possible that pancreatic acinar cells can be exposed to insulin levels of this magnitude in situ.
D000818:Animals; D002241:Carbohydrates / Q000494:pharmacology; D002766:Cholecystokinin / Q000494:pharmacology*; D004357:Drug Synergism; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism*; D010189:Pancreatic Juice / Q000378:metabolism; D051381:Rats
D002241:Carbohydrates; D007328:Insulin; D002766:Cholecystokinin; D005947:Glucose