Control of insulin secretion by catecholamines, stress, and the sympathetic nervous system

Catecholamines inhibit insulin release by stimulation of a pancreatic α receptor. Catecholamines stimulate insulin release by stimulation of a pancreatic β receptor. α Receptor activity tends to decrease intracellular cyclic AMP and β receptor activity tends to increase intracellular cyclic AMP. β Receptor stimulation of insulin secretion probably involves generation of cyclic AMP, but α receptor stimulation has a major inhibitory effect on insulin release independent of its ability to diminish intracellular cyclic AMP. Activation of the sympathetic nervous system causes inhibition of glucose stimulated insulin secretion via the α receptor, but insulin output is maintained, probably via simultaneous β receptor stimulation. This dual islet function of catecholamines can be related to a 2 pool model for the regulation of insulin secretion by glucose. Pathological stress states may induce a metabolic state similar to diabetes with hyperglycemia and poor insulin responses to glucose challenge. Cntral nervous system input to the endocrine pancreas following environmental stimuli seems likely.