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

D. Porte, R. P. Robertson

Research output: Contribution to journalReview articlepeer-review

174 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1792-1796
Number of pages5
JournalFederation Proceedings
Volume32
Issue number7
StatePublished - Dec 1 1973

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