Pj. Havel et al., AUTONOMIC CONTROL OF PANCREATIC-POLYPEPTIDE AND GLUCAGON-SECRETION DURING NEUROGLUCOPENIA AND HYPOGLYCEMIA IN MICE, The American journal of physiology, 265(1), 1993, pp. 180000246-180000254
Neural control of pancreatic polypeptide (PP) release has not been pre
viously investigated in the mouse. In addition, it is not known to wha
t extent increased glucagon secretion during hypoglycemia in mice is n
eurally mediated vs. an effect of hypoglycemia to directly stimulate g
lucagon secretion at the level of the islet. Feeding or the cholinergi
c agonist carbachol increased plasma PP levels in conscious mice (+74
+/- 18 pg/ml vs. fasted mice and +141 +/- 17 pg/ml vs. control, respec
tively). Neuroglucopenia induced by 2-deoxy-D-glucose or insulin-induc
ed hypoglycemia also increased plasma PP (+79 +/- 18 and +89 +/- 11 pg
/ml vs. control, respectively). These increases were abolished by hexa
methonium and reduced by atropine methylnitrate (atropine). Hypoglycem
ia-induced hyperglucagonemia (+1,243 +/- 275 pg/ml) was reduced to 31
+/- 7% of control by atropine (+382 +/- 85 pg/ml), to 48 +/- 9% of con
trol by combined adrenergic blockade (+601 +/- 112 pg/ml), and nearly
abolished by atropine plus combined blockade (+143 +/- 41 pg/ml; 11 +/
- 3% of control) or hexamethonium (+151 +/- 38 pg/ml; 12 +/- 3% of con
trol). We conclude the following in the mouse. 1) Feeding or cholinerg
ic agonists increase plasma PP. 2) During neuroglucopenia or hypoglyce
mia, plasma PP is increased via nicotinic and muscarinic mechanisms. 3
) The glucagon response to hypoglycemia is predominantly the result of
autonomic activation and is mediated by both muscarinic and adrenergi
c mechanisms.