Minireview: Dopaminergic Regulation of Insulin Secretion from the Pancreatic Islet
Identifieur interne : 000322 ( Pmc/Corpus ); précédent : 000321; suivant : 000323Minireview: Dopaminergic Regulation of Insulin Secretion from the Pancreatic Islet
Auteurs : Alessandro Ustione ; David W. Piston ; Paul E. HarrisSource :
- Molecular Endocrinology [ 0888-8809 ] ; 2013.
Abstract
Exogenous dopamine inhibits insulin secretion from pancreatic β-cells, but the lack of dopaminergic neurons in pancreatic islets has led to controversy regarding the importance of this effect. Recent data, however, suggest a plausible physiologic role for dopamine in the regulation of insulin secretion. We review the literature underlying our current understanding of dopaminergic signaling that can down-regulate glucose-stimulated insulin secretion from pancreatic islets. In this negative feedback loop, dopamine is synthesized in the β-cells from circulating
Url:
DOI: 10.1210/me.2013-1083
PubMed: 23744894
PubMed Central: 3725340
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PMC:3725340Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Minireview: Dopaminergic Regulation of Insulin Secretion from the Pancreatic Islet</title><author><name sortKey="Ustione, Alessandro" sort="Ustione, Alessandro" uniqKey="Ustione A" first="Alessandro" last="Ustione">Alessandro Ustione</name></author><author><name sortKey="Piston, David W" sort="Piston, David W" uniqKey="Piston D" first="David W." last="Piston">David W. Piston</name></author><author><name sortKey="Harris, Paul E" sort="Harris, Paul E" uniqKey="Harris P" first="Paul E." last="Harris">Paul E. Harris</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23744894</idno><idno type="pmc">3725340</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725340</idno><idno type="RBID">PMC:3725340</idno><idno type="doi">10.1210/me.2013-1083</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000322</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000322</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Minireview: Dopaminergic Regulation of Insulin Secretion from the Pancreatic Islet</title><author><name sortKey="Ustione, Alessandro" sort="Ustione, Alessandro" uniqKey="Ustione A" first="Alessandro" last="Ustione">Alessandro Ustione</name></author><author><name sortKey="Piston, David W" sort="Piston, David W" uniqKey="Piston D" first="David W." last="Piston">David W. Piston</name></author><author><name sortKey="Harris, Paul E" sort="Harris, Paul E" uniqKey="Harris P" first="Paul E." last="Harris">Paul E. Harris</name></author></analytic><series><title level="j">Molecular Endocrinology</title><idno type="ISSN">0888-8809</idno><idno type="eISSN">1944-9917</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Exogenous dopamine inhibits insulin secretion from pancreatic β-cells, but the lack of dopaminergic neurons in pancreatic islets has led to controversy regarding the importance of this effect. Recent data, however, suggest a plausible physiologic role for dopamine in the regulation of insulin secretion. We review the literature underlying our current understanding of dopaminergic signaling that can down-regulate glucose-stimulated insulin secretion from pancreatic islets. In this negative feedback loop, dopamine is synthesized in the β-cells from circulating <sc>l</sc>-dopa, serves as an autocrine signal that is cosecreted with insulin, and causes a tonic inhibition on glucose-stimulated insulin secretion. On the whole animal scale, <sc>l</sc>-dopa is produced by cells in the gastrointestinal tract, and its concentration in the blood plasma increases following a mixed meal. By reviewing the outcome of certain types of bariatric surgery that result in rapid amelioration of glucose tolerance, we hypothesize that dopamine serves as an “antiincretin” signal that counterbalances the stimulatory effect of glucagon-like peptide 1.</p></div></front></TEI><pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Mol Endocrinol</journal-id><journal-id journal-id-type="iso-abbrev">Mol. Endocrinol</journal-id><journal-id journal-id-type="hwp">mend</journal-id><journal-id journal-id-type="publisher-id">molen</journal-id><journal-id journal-id-type="pmc">mend</journal-id><journal-title-group><journal-title>Molecular Endocrinology</journal-title></journal-title-group><issn pub-type="ppub">0888-8809</issn><issn pub-type="epub">1944-9917</issn><publisher><publisher-name>Endocrine Society</publisher-name><publisher-loc>Chevy Chase, MD</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23744894</article-id><article-id pub-id-type="pmc">3725340</article-id><article-id pub-id-type="publisher-id">ME-13-1083</article-id><article-id pub-id-type="doi">10.1210/me.2013-1083</article-id><article-categories><subj-group subj-group-type="heading"><subject>Minireviews</subject></subj-group></article-categories><title-group><article-title>Minireview: Dopaminergic Regulation of Insulin Secretion from the Pancreatic Islet</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Ustione</surname><given-names>Alessandro</given-names></name></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Piston</surname><given-names>David W.</given-names></name></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Harris</surname><given-names>Paul E.</given-names></name></contrib><aff>Department of Molecular Physiology and Biophysics (A.U., D.W.P.), Vanderbilt University, Nashville, Tennessee 37232; and Department of Medicine (P.E.H.), Columbia University, New York, New York 10032</aff></contrib-group><author-notes><corresp>Address all correspondence and requests for reprints to: David W. Piston, <addr-line>Department of Molecular Physiology and Biophysics, Vanderbilt University, 702 Light Hall, Nashville, Tennessee 37232-0615.</addr-line> E-mail: <email>Dave.Piston@Vanderbilt.edu</email>; or Paul E. Harris, <addr-line>Department of Medicine, Columbia University, 650 West 168th Street, BB20–06, New York, New York 10032-3702.</addr-line> E-mail: <email>peh1@columbia.edu</email>.</corresp></author-notes><pub-date pub-type="ppub"><month>8</month><year>2013</year></pub-date><pub-date pub-type="epub"><day>6</day><month>6</month><year>2013</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>8</month><year>2014</year></pub-date><pmc-comment> PMC Release delay is 12 months and
0 days and was based on the
<volume>27</volume><issue>8</issue><fpage>1198</fpage><lpage>1207</lpage><history><date date-type="received"><day>4</day><month>4</month><year>2013</year></date><date date-type="accepted"><day>29</day><month>5</month><year>2013</year></date></history><permissions><copyright-statement>Copyright © 2013 by The Endocrine Society</copyright-statement><copyright-year>2013</copyright-year></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zmg00813001198.pdf"></self-uri><abstract><p>Exogenous dopamine inhibits insulin secretion from pancreatic β-cells, but the lack of dopaminergic neurons in pancreatic islets has led to controversy regarding the importance of this effect. Recent data, however, suggest a plausible physiologic role for dopamine in the regulation of insulin secretion. We review the literature underlying our current understanding of dopaminergic signaling that can down-regulate glucose-stimulated insulin secretion from pancreatic islets. In this negative feedback loop, dopamine is synthesized in the β-cells from circulating <sc>l</sc>-dopa, serves as an autocrine signal that is cosecreted with insulin, and causes a tonic inhibition on glucose-stimulated insulin secretion. On the whole animal scale, <sc>l</sc>-dopa is produced by cells in the gastrointestinal tract, and its concentration in the blood plasma increases following a mixed meal. By reviewing the outcome of certain types of bariatric surgery that result in rapid amelioration of glucose tolerance, we hypothesize that dopamine serves as an “antiincretin” signal that counterbalances the stimulatory effect of glucagon-like peptide 1.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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