Abstract
Insulin release from the perfused pancreas was studied in genetically selected fat and lean chickens. The previously described glucose insensitivity of the chicken pancreas cannot be overcome by 5 or 10 mM D-glyceraldehyde, suggesting that the resistance is not related to glucose metabolism before the triose phosphate step. At 42 mM, glucose induced a biphasic insulin release which was specific, since 42 mM mannitol did not elicit insulin release. Arginine (10 mM) or acetylcholine (0.1-1 microM), which in themselves do not cause insulin release, generated a biphasic insulin release in the presence of a low nonstimulating glucose concentration (14 mM); the effect was synergistic. In contrast to the glucose tolerance test observed in vivo, the pancreas from the fat line chicken in response to glucose or glucose plus arginine released significantly less insulin during the first phase. The significance of this defect awaits further elucidation. On the other hand, acetylcholine, a more potent secretagogue, did not reveal any significant difference between fat and lean chickens.
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