Corticotropin-releasing factor inhibits insulin release from perfused rat pancreas.
The ability of synthetic corticotropin-releasing factor (CRF) (rat) to influence hormone release from the endocrine pancreas of rats has been evaluated by means of perfusion in situ. Release of insulin and glucagon into the perfusate was measured in the presence and absence of CRF (0.1, 1, and 10 ng/ml) under conditions of normal and high glucose concentration (5.5 and 11 mM). Under both conditions, CRF (0.1, 1, and 10 ng/ml) induced a rapid, dose-dependent inhibition of insulin release followed by a remarkable postinhibitory rebound when exposure to CRF was discontinued. CRF had no significant effect on glucagon release when tested under these conditions. These results are reminiscent of noradrenergic inhibition of insulin release and together with evidence for the presence of CRF in the pancreas suggest that this peptide could function as a neuromodulatory transducer in addition to its role as a hypophysiotropic hormone perhaps contributing to the coordination of the overall endocrine response to stress.
D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology* / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005934:Glucagon / Q000378:metabolism; D007328:Insulin / Q000378:metabolism*; D007329:Insulin Antagonists / Q000494:pharmacology; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D007329:Insulin Antagonists; D005934:Glucagon; D003346:Corticotropin-Releasing Hormone