Meal-induced insulin secretion in dogs is mediated by both branches of theautonomic nervous system

Citation
L. Benthem et al., Meal-induced insulin secretion in dogs is mediated by both branches of theautonomic nervous system, AM J P-ENDO, 278(4), 2000, pp. E603-E610
Citations number
42
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
ISSN journal
01931849 → ACNP
Volume
278
Issue
4
Year of publication
2000
Pages
E603 - E610
Database
ISI
SICI code
0193-1849(200004)278:4<E603:MISIDI>2.0.ZU;2-2
Abstract
We investigated the relationship between autonomic activity to the pancreas and insulin secretion in chronically catheterized dogs when food was shown , during eating, and during the early absorptive period. Pancreatic polypep tide (PP) output, pancreatic norepinephrine spillover (PNESO), and arterial epinephrine (Epi) were measured as indexes for parasympathetic and sympath etic nervous activity to the pancreas and for adrenal medullary activity, r espectively. The relation between autonomic activity and insulin secretion was confirmed by autonomic blockade. Showing food to dogs initiated a trans ient increase in insulin secretion without changing PP output or PNESO. Epi did increase, suggesting beta(2)-adrenergic mediation, which was confirmed by beta-adrenoceptor blockade. Eating initiated a second transient insulin response, which was only totally abolished by combined muscarinic and beta -adrenoceptor blockade. During absorption, insulin increased to a plateau. PP output showed the same pattern, suggesting parasympathetic mediation. PN ESO decreased by 50%, suggesting withdrawal of inhibitory sympathetic neura l tone. We conclude that 1) the insulin response to showing food is mediate d by the beta(2)-adrenergic effect of Epi, 2) the insulin response to eatin g is mediated both by parasympathetic muscarinic stimulation and by the bet a(2)-adrenergic effect of Epi, and 3) the insulin response during early abs orption is mediated by parasympathetic activation, with possible contributi on of withdrawal of sympathetic neural tone.