Evidence for noncholinergic ganglionic neural stimulation of B cell secretion

Insulin levels increase after 2-deoxyglucose (2DG) administration in dogs. This observation is in contrast to the decrease in insulin level post-2DG in baboons and rabbits. To evaluate a possible neural mechanism mediating this increase in insulin level, the authors studied normal mongrel dogs with 2DG alone, 2DG during ganglionic blockade, beta -adrenergic blockade, and postganglionic parasympathetic blockade. There was an increase in plasma epinephrine, norepinephrine, pancreatic polypeptide, insulin, and glucose post-2DG alone. During ganglionic blockade, the increase in epinephrine, norepinephrine, and pancreatic polypeptide post-2DG was completely abolished, verifying ganglionic blockade of sympathetic and parasympathetic pathways, respectively. The data suggests that the insulin rise post-2DG is beta -adrenergic, but the ganglionic neurotransmitter mediating the 2DG-induced insulin rise during ganglionic blockade is noncholinergic (possibly peptidergic).