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Diabetes, Vol 37, Issue 9 1157-1162, Copyright © 1988 by American Diabetes Association
Galanin--sympathetic neurotransmitter in endocrine pancreas?
BE Dunning and GJ Taborsky
Department of Medicine, University of Washington, Seattle.
The effects of sympathetic neural activation on basal pancreatic hormone
secretion cannot be explained solely by the actions of the classic
sympathetic neurotransmitter norepinephrine. The nonadrenergic component
may be mediated by the 29-amino acid peptide galanin in that this
neuropeptide meets several of the criteria necessary to be considered a
sympathetic neurotransmitter in the endocrine pancreas. 1) Galanin
administration inhibits basal insulin and somatostatin secretion and
stimulates basal glucagon secretion from the pancreas, qualitatively
reproducing the effects of sympathetic nerve stimulation. These
sympathomimetic effects appear to be mediated by direct actions of galanin
on the islet. 2) Galanin-like immunoreactivity exists in fibers that
innervate pancreatic islets. 3) Galanin is released during electrical
stimulation of pancreatic nerves. The quantity released is sufficient to
reproduce sympathetic nerve stimulation-induced effects on insulin
secretion and to contribute to the neural effects on somatostatin and
glucagon release. 4) Whether interference with galanin action or release
reduces the islet response to sympathetic nerve stimulation remains to be
determined. We hypothesize that galanin and norepinephrine act together to
mediate the islet response to sympathetic neural activation. If galanin is
a sympathetic neurotransmitter in the endocrine pancreas, it may contribute
to the inhibition of insulin secretion that occurs during stress and
thereby to the hyperglycemic response. Moreover, the local presence of this
potent beta-cell inhibitor in the islet leads to speculation on galanin's
contribution to the impairment of insulin secretion that occurs in
non-insulin-dependent diabetes mellitus and therefore on the potential
utility of a galanin antagonist in the treatment of this disease.

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Copyright © 1988 by the American Diabetes Association.
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