Glucose, beta adrenergic effects, and pancreatic endocrine function in the isolated perfused duck pancreas.
Duck isolated perfused pancreas was used to assess glucose, adrenergic mediated effects and pancreatic function interrelationships. A moderate physiological 50% increase in glucose level, corresponding closely to the difference observed between 24-h-fasted and fed animals, induced a significant decrease of pancreatic glucagon not due to a rise in somatostatin secretion. The great responsiveness of the A cell was still found after glucagon stimulation by catecholamines or beta adrenergic agonism. Insulin was irresponsive to the glucose load we used, suggesting that glucose-induced glucagon suppression was also insulin independent. As far as the D cell was concerned, glucose had no effect on pancreatic somatostatin output; however, an interesting finding was that beta adrenergic agonism has a permissive effect on D cell responsiveness to the nutriment.
D000818:Animals; D004372:Ducks; D004837:Epinephrine / Q000494:pharmacology; D005934:Glucagon / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D010477:Perfusion; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000187:drug effects*; D013004:Somatostatin / Q000494:pharmacology
D007328:Insulin; D011943:Receptors, Adrenergic, beta; D013004:Somatostatin; D005934:Glucagon; D011433:Propranolol; D005947:Glucose; D009638:Norepinephrine; D004837:Epinephrine; D010646:Phentolamine