CAMP AND OR ACETYLCHOLINE PERMIT AN INSULIN-RESPONSE TO FUEL NUTRIENTS IN CHICKEN/

1. The possibility that 8-bromo cyclic adenosine monophosphate (8-Br-c AMP) or acetylcholine (ACh) potentiates insulin release in chicken pan creas in response to D-glyceraldehyde (D-GA, a weak insulinotropic fue l), and permits an insulin release in response to D-mannose or alpha-k etoisocaproic acid (ar-KIC) (two non-insulinotropic fuels in chicken p ancreas) is examined. 2. 8-Br-cAMP(I mM) or ACh(l mu M) permitted a su stained although delayed insulin release in response to D-GA (5 and 15 mM). 3. The resistance to D-mannose (50 mM) or alpha KIC (1O mM) pers isted in the presence of 8-Br-cAMP. 4. At 1 or 100 mu M, ACh permitted a slight, immediate and transient insulin output in response to c(-KI C but not to D-mannose (with one unexplained exception). 5. The simult aneous perfusion of 8-Br-cAMP + ACh increased the basal rate of insuli n release, and permitted a large and sustained response to D-mannose. It also greatly increased the immediate response to alpha-KIC + ACh. 6 . In conclusion. in chicken pancreas fuel nutrients require the activa tion 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.