AJP - Endocrinology and Metabolism, Vol 257, Issue 1 E15-E19, Copyright © 1989 by American Physiological Society

ARTICLES

L-leucine or its keto acid potentiate but do not initiate insulin release in chicken

N. Rideau and J. Simon
Station de Recherches Avicoles, Institut National de la Recherche Agronomique de Nouzilly, Monnaie, France.

In the isolated perfused chicken pancreas, 20 and 40 mM L-leucine or 10-40 mM alpha-ketoisocaproic acid (alpha-KIC) did not initiate insulin release. In the presence of 14 mM glucose (a noninsulinotropic concentration), 20 mM L-leucine and 10 mM alpha-KIC evoked a slight biphasic insulin release. The response to 20 mM L-leucine was further increased when 14 mM glucose was combined with 10 mM L-glutamine (10 mM glutamine alone did not induce insulin release and did not potentiate the response to 10 mM L-leucine). At 1 mM, 8-bromo-adenosine 3',5'-cyclic monophosphate (8-BrcAMP) alone caused a slight and progressive increase in insulin secretion but did not sensitize the pancreas to either 20 mM L-leucine or 10 mM alpha-KIC, whereas it facilitated a marked insulin release in response to 14 mM glucose. On the other hand, 10-40 mM K+ or 20 mM L-arginine induced a rapid monophasic insulin output. In conclusion, L-leucine or alpha-KIC, which do not initiate insulin release alone and are not potentiated by 8-BrcAMP, may not be regarded as primary insulinotropic agents in the chicken. This result, together with the previously documented resistance of the chicken pancreas to glucose alone or to D-glyceraldehyde, strongly suggests that the mechanisms initiating insulin secretion are different in chickens and mammals, whereas potentiating mechanisms (low glucose concentration, arginine, acetylcholine, and cAMP) and membrane depolarization events (K+ and arginine) are present in both chickens and mammals.