Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/69464
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dc.contributor.authorMontanya Mias, Eduard-
dc.date.accessioned2016-02-16T16:16:06Z-
dc.date.available2016-02-16T16:16:06Z-
dc.date.issued2014-03-15-
dc.identifier.issn0012-1797-
dc.identifier.urihttp://hdl.handle.net/2445/69464-
dc.description.abstractThe global epidemic of type 2 diabetes is largely secondary to insulin resistance induced by obesity and sedentary lifestyles. Most insulin-resistant subjects are able to increase b-cell secretion to meet the increased insulin demand and do not develop diabetes. However, when b-cell compensation fails, type 2 diabetes develops (1,2). Understanding the mechanisms of this compensatory response is of fundamental importance to elucidate the pathophysiology of type 2 diabetes and has implications for the treatment of the disease.-
dc.format.extent3 p.-
dc.format.mimetypeapplication/pdf-
dc.language.isoeng-
dc.publisherAmerican Diabetes Association-
dc.relation.isformatofReproducció del document publicat a: http://dx.doi.org/10.2337/db13-1843-
dc.relation.ispartofDiabetes, 2014, vol. 63, num. 3, p. 832-834-
dc.relation.urihttp://dx.doi.org/10.2337/db13-1843-
dc.rightscc-by-nc-nd (c) American Diabetes Association, 2014-
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es-
dc.sourceArticles publicats en revistes (Ciències Clíniques)-
dc.subject.classificationResistència a la insulina-
dc.subject.classificationIllots de Langerhans-
dc.subject.otherInsulin resistance-
dc.subject.otherIslands of Langerhans-
dc.titleInsulin resistance compensation: not just a beta cell matter?-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.identifier.idgrec656809-
dc.date.updated2016-02-16T16:16:06Z-
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess-
Appears in Collections:Articles publicats en revistes (Ciències Clíniques)

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