CAMP and/or acetylcholine permit an insulin response to fuel nutrients in chicken

Abstract

1. 1. The possibility that 8-bromo cyclic adenosine monophosphate (8-Br-cAMP) or acetylcholine (ACh) potentiates insulin release in chicken pancreas in response to d-glyceraldehyde (D-GA, a weak insulinotropic fuel), and permits an insulin release in response to D-mannose or α-ketoisocaproic acid (α-KIC) (two non-insulinotropic fuels in chicken pancreas) is examined. 2. 2.8-Br-cAMP (1 mM) or ACh (1 μM) permitted a sustained although delayed insulin release in response to D-GA (5 and 15mM). 3. 3. The resistance to D-mannose (50 mM) or α-KIC (10 mM) persisted in the presence of 8-Br-cAMP. 4. 4. At 1 or 100 μM, ACh permitted a slight, immediate and transient insulin output in response to α-KIC but not to d-mannose (with one unexplained exception). 5. 5. The simultaneous perfusion of 8-Br-cAMP + ACh increased the basal rate of insulin release, and permitted a large and sustained response to D-mannose. It also greatly increased the immediate response to α-KIC + ACh. 6. 6. In conclusion, in chicken pancreas fuel nutrients require the activation of cAMP- and/or ACh-dependent pathways to induce insulin release. Whether this peculiarity is related to the high glycemia of chickens awaits further investigation.