MicroRNAs contribute to compensatory β cell expansion during pregnancy and obesity
Identifieur interne : 000F83 ( Ncbi/Merge ); précédent : 000F82; suivant : 000F84MicroRNAs contribute to compensatory β cell expansion during pregnancy and obesity
Auteurs : Cécile Jacovetti [Suisse] ; Amar Abderrahmani [France] ; Géraldine Parnaud [Suisse] ; Jean-Christophe Jonas [Belgique] ; Marie-Line Peyot [Canada] ; Marion Cornu [Suisse] ; Ross Laybutt [Australie] ; Emmanuelle Meugnier [France] ; Sophie Rome [France] ; Bernard Thorens [Suisse] ; Marc Prentki [Canada] ; Domenico Bosco [Suisse] ; Romano Regazzi [Suisse]Source :
- The Journal of Clinical Investigation [ 0021-9738 ] ; 2012.
Abstract
Pregnancy and obesity are frequently associated with diminished insulin sensitivity, which is normally compensated for by an expansion of the functional β cell mass that prevents chronic hyperglycemia and development of diabetes mellitus. The molecular basis underlying compensatory β cell mass expansion is largely unknown. We found in rodents that β cell mass expansion during pregnancy and obesity is associated with changes in the expression of several islet microRNAs, including miR-338-3p. In isolated pancreatic islets, we recapitulated the decreased miR-338-3p level observed in gestation and obesity by activating the G protein–coupled estrogen receptor GPR30 and the glucagon-like peptide 1 (GLP1) receptor. Blockade of miR-338-3p in β cells using specific anti-miR molecules mimicked gene expression changes occurring during β cell mass expansion and resulted in increased proliferation and improved survival both in vitro and in vivo. These findings point to a major role for miR-338-3p in compensatory β cell mass expansion occurring under different insulin resistance states.
Url:
DOI: 10.1172/JCI64151
PubMed: 22996663
PubMed Central: 3461923
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<front><div type="abstract" xml:lang="en"><p>Pregnancy and obesity are frequently associated with diminished insulin sensitivity, which is normally compensated for by an expansion of the functional β cell mass that prevents chronic hyperglycemia and development of diabetes mellitus. The molecular basis underlying compensatory β cell mass expansion is largely unknown. We found in rodents that β cell mass expansion during pregnancy and obesity is associated with changes in the expression of several islet microRNAs, including miR-338-3p. In isolated pancreatic islets, we recapitulated the decreased miR-338-3p level observed in gestation and obesity by activating the G protein–coupled estrogen receptor GPR30 and the glucagon-like peptide 1 (GLP1) receptor. Blockade of miR-338-3p in β cells using specific anti-miR molecules mimicked gene expression changes occurring during β cell mass expansion and resulted in increased proliferation and improved survival both in vitro and in vivo. These findings point to a major role for miR-338-3p in compensatory β cell mass expansion occurring under different insulin resistance states.</p>
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<contrib-group><contrib contrib-type="author"><name><surname>Jacovetti</surname>
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<xref ref-type="aff" rid="JCI64151">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Abderrahmani</surname>
<given-names>Amar</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Parnaud</surname>
<given-names>Géraldine</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Jonas</surname>
<given-names>Jean-Christophe</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Peyot</surname>
<given-names>Marie-Line</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">5</xref>
<xref ref-type="aff" rid="JCI64151">6</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cornu</surname>
<given-names>Marion</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">7</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Laybutt</surname>
<given-names>Ross</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">8</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Meugnier</surname>
<given-names>Emmanuelle</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">9</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Rome</surname>
<given-names>Sophie</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">9</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Thorens</surname>
<given-names>Bernard</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">7</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Prentki</surname>
<given-names>Marc</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">5</xref>
<xref ref-type="aff" rid="JCI64151">6</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bosco</surname>
<given-names>Domenico</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Regazzi</surname>
<given-names>Romano</given-names>
</name>
<xref ref-type="aff" rid="JCI64151">1</xref>
</contrib>
</contrib-group>
<aff id="JCI64151"><label>1</label>
Department of Cell Biology and Morphology, University of Lausanne, Lausanne, Switzerland.<label>2</label>
University of Lille Nord de France, European Genomic Institute for Diabetes EGID FR 3508, UMR 8199, Lille, France.<label>3</label>
Cell Isolation and Transplantation Center, Department of Surgery, Geneva University Hospitals and University of Geneva, Geneva, Switzerland.<label>4</label>
Université catholique de Louvain, Institut de recherche expérimentale et clinique, Pôle d’endocrinologie, diabète et nutrition, Brussels, Belgium.<label>5</label>
Montreal Diabetes Research Center and CRCHUM, Montreal, Quebec, Canada.<label>6</label>
Departments of Nutrition and Biochemistry, University of Montreal, Montreal, Quebec, Canada.<label>7</label>
Center for Integrative Genomics, University of Lausanne, Genopode Building, Lausanne, Switzerland.<label>8</label>
Diabetes and Obesity Research Program, Garvan Institute of Medical Research, St. Vincent’s Hospital, Sydney, New South Wales, Australia.<label>9</label>
Laboratory CarMen (INSERM 1060, INRA 1235, INSA), University of Lyon, Faculté de Médecine Lyon-Sud, Chemin du Grand Revoyet, Oullins, France.</aff>
<author-notes><corresp>Address correspondence to: Romano Regazzi, Department of Cell Biology and Morphology, Rue du Bugnon 9, 1005 Lausanne, Lausanne, Switzerland. Phone: 41.21.692.52.80; Fax: 41.21.692.52.55; E-mail:
<email>Romano.Regazzi@unil.ch</email>
.
</corresp>
</author-notes>
<pub-date pub-type="epub"><day>10</day>
<month>9</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="ppub"><day>1</day>
<month>10</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>10</day>
<month>9</month>
<year>2012</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
. </pmc-comment>
<volume>122</volume>
<issue>10</issue>
<fpage>3541</fpage>
<lpage>3551</lpage>
<history><date date-type="received"><day>4</day>
<month>4</month>
<year>2012</year>
</date>
<date date-type="accepted"><day>19</day>
<month>7</month>
<year>2012</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2012, American Society for Clinical Investigation</copyright-statement>
<copyright-year>2012</copyright-year>
</permissions>
<abstract><p>Pregnancy and obesity are frequently associated with diminished insulin sensitivity, which is normally compensated for by an expansion of the functional β cell mass that prevents chronic hyperglycemia and development of diabetes mellitus. The molecular basis underlying compensatory β cell mass expansion is largely unknown. We found in rodents that β cell mass expansion during pregnancy and obesity is associated with changes in the expression of several islet microRNAs, including miR-338-3p. In isolated pancreatic islets, we recapitulated the decreased miR-338-3p level observed in gestation and obesity by activating the G protein–coupled estrogen receptor GPR30 and the glucagon-like peptide 1 (GLP1) receptor. Blockade of miR-338-3p in β cells using specific anti-miR molecules mimicked gene expression changes occurring during β cell mass expansion and resulted in increased proliferation and improved survival both in vitro and in vivo. These findings point to a major role for miR-338-3p in compensatory β cell mass expansion occurring under different insulin resistance states.</p>
</abstract>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Australie</li>
<li>Belgique</li>
<li>Canada</li>
<li>France</li>
<li>Suisse</li>
</country>
<region><li>Canton de Vaud</li>
<li>Hauts-de-France</li>
<li>Nord-Pas-de-Calais</li>
<li>Région de Bruxelles-Capitale</li>
</region>
<settlement><li>Bruxelles</li>
<li>Lausanne</li>
<li>Lille</li>
<li>Louvain-la-Neuve</li>
</settlement>
<orgName><li>Université catholique de Louvain</li>
</orgName>
</list>
<tree><country name="Suisse"><region name="Canton de Vaud"><name sortKey="Jacovetti, Cecile" sort="Jacovetti, Cecile" uniqKey="Jacovetti C" first="Cécile" last="Jacovetti">Cécile Jacovetti</name>
</region>
<name sortKey="Bosco, Domenico" sort="Bosco, Domenico" uniqKey="Bosco D" first="Domenico" last="Bosco">Domenico Bosco</name>
<name sortKey="Cornu, Marion" sort="Cornu, Marion" uniqKey="Cornu M" first="Marion" last="Cornu">Marion Cornu</name>
<name sortKey="Parnaud, Geraldine" sort="Parnaud, Geraldine" uniqKey="Parnaud G" first="Géraldine" last="Parnaud">Géraldine Parnaud</name>
<name sortKey="Regazzi, Romano" sort="Regazzi, Romano" uniqKey="Regazzi R" first="Romano" last="Regazzi">Romano Regazzi</name>
<name sortKey="Thorens, Bernard" sort="Thorens, Bernard" uniqKey="Thorens B" first="Bernard" last="Thorens">Bernard Thorens</name>
</country>
<country name="France"><region name="Hauts-de-France"><name sortKey="Abderrahmani, Amar" sort="Abderrahmani, Amar" uniqKey="Abderrahmani A" first="Amar" last="Abderrahmani">Amar Abderrahmani</name>
</region>
<name sortKey="Meugnier, Emmanuelle" sort="Meugnier, Emmanuelle" uniqKey="Meugnier E" first="Emmanuelle" last="Meugnier">Emmanuelle Meugnier</name>
<name sortKey="Rome, Sophie" sort="Rome, Sophie" uniqKey="Rome S" first="Sophie" last="Rome">Sophie Rome</name>
</country>
<country name="Belgique"><region name="Région de Bruxelles-Capitale"><name sortKey="Jonas, Jean Christophe" sort="Jonas, Jean Christophe" uniqKey="Jonas J" first="Jean-Christophe" last="Jonas">Jean-Christophe Jonas</name>
</region>
</country>
<country name="Canada"><noRegion><name sortKey="Peyot, Marie Line" sort="Peyot, Marie Line" uniqKey="Peyot M" first="Marie-Line" last="Peyot">Marie-Line Peyot</name>
</noRegion>
<name sortKey="Peyot, Marie Line" sort="Peyot, Marie Line" uniqKey="Peyot M" first="Marie-Line" last="Peyot">Marie-Line Peyot</name>
<name sortKey="Prentki, Marc" sort="Prentki, Marc" uniqKey="Prentki M" first="Marc" last="Prentki">Marc Prentki</name>
<name sortKey="Prentki, Marc" sort="Prentki, Marc" uniqKey="Prentki M" first="Marc" last="Prentki">Marc Prentki</name>
</country>
<country name="Australie"><noRegion><name sortKey="Laybutt, Ross" sort="Laybutt, Ross" uniqKey="Laybutt R" first="Ross" last="Laybutt">Ross Laybutt</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>
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