Insulin resistance compensation: not just a beta cell matter?

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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.date.updated2016-02-16T16:16:06Z
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.identifier.idgrec656809
dc.identifier.issn0012-1797
dc.identifier.urihttps://hdl.handle.net/2445/69464
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.accessRightsinfo:eu-repo/semantics/openAccess
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

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