Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/176349
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dc.contributor.authorBotteri, Gaiaes_ES
dc.contributor.authorMontori, Martaes_ES
dc.contributor.authorGumà, Annaes_ES
dc.contributor.authorPizarro, Javieres_ES
dc.contributor.authorCedó, Lídiaes_ES
dc.contributor.authorEscolà-Gil, Joan Carleses_ES
dc.contributor.authorLi, Dianaes_ES
dc.contributor.authorBarroso, Emmaes_ES
dc.contributor.authorKohan, Alison B.es_ES
dc.contributor.authorVázquez-Carrera, Manueles_ES
dc.date.accessioned2019-02-19T08:43:04Z-
dc.date.available2019-02-19T08:43:04Z-
dc.date.issued2017-11-
dc.identifier.citationDiabetologia 60(11): 2262–2273 (2017)es_ES
dc.identifier.issn0012-186X-
dc.identifier.issn10.1007/s00125-017-4401-5-
dc.identifier.urihttp://hdl.handle.net/10261/176349-
dc.description.abstract[Aim/hypothesis] Here, our aim was to examine whether VLDL and apolipoprotein (apo) CIII induce endoplasmic reticulum (ER) stress, inflammation and insulin resistance in skeletal muscle. [Methods] Studies were conducted in mouse C2C12 myotubes, isolated skeletal muscle and skeletal muscle from transgenic mice overexpressing apoCIII. [Results] C2C12 myotubes exposed to VLDL showed increased levels of ER stress and inflammatory markers whereas peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) and AMP-activated protein kinase (AMPK) levels were reduced and the insulin signalling pathway was attenuated. The effects of VLDL were also observed in isolated skeletal muscle incubated with VLDL. The changes caused by VLDL were dependent on extracellular signal-regulated kinase (ERK) 1/2 since they were prevented by the ERK1/2 inhibitor U0126 or by knockdown of this kinase by siRNA transfection. ApoCIII mimicked the effects of VLDL and its effects were also blocked by ERK1/2 inhibition, suggesting that this apolipoprotein was responsible for the effects of VLDL. Skeletal muscle from transgenic mice overexpressing apoCIII showed increased levels of some ER stress and inflammatory markers and increased phosphorylated ERK1/2 levels, whereas PGC-1α levels were reduced, confirming apoCIII effects in vivo. Finally, incubation of myotubes with a neutralising antibody against Toll-like receptor 2 abolished the effects of apoCIII on ER stress, inflammation and insulin resistance, indicating that the effects of apoCIII were mediated by this receptor. [Conclusions/interpretation] These results imply that elevated VLDL in diabetic states can contribute to the exacerbation of insulin resistance by activating ERK1/2 through Toll-like receptor 2.es_ES
dc.description.sponsorshipThis study was partly supported by funds from the Spanish Ministerio de Economía y Competitividad (SAF2012-30708 and SAF2015-64146-R to MVC), the Generalitat de Catalunya (2014SGR0013 to MVC), NIH NIDDK (DK101663 to ABK), USDA NIFA (11874590 to ABK) and USDA NIFA Hatch Formula Funds (2015- 31200-06009 to ABK), an Instituto de Salud Carlos III grant (PI16- 00139 to JCE-G) and European Union ERDF funds. CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) is an Instituto de Salud Carlos III project (Grant CB07/08/0003 to MVC). GB was supported by an FPI grant from the Spanish Ministerio de Economía y Competitividad.es_ES
dc.language.isoenges_ES
dc.publisherSpringeres_ES
dc.relationMINECO/ICTI2013-2016/SAF2015-64146-Res_ES
dc.rightsclosedAccesses_ES
dc.subjectAMPKes_ES
dc.subjectapoCIIIes_ES
dc.subjectERK1/2es_ES
dc.subjectTLR2es_ES
dc.subjectVLDLes_ES
dc.titleVLDL and apolipoprotein CIII induce ER stress and inflammation and attenuate insulin signalling via Toll-like receptor 2 in mouse skeletal muscle cellses_ES
dc.typeartículoes_ES
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1007/s00125-017-4401-5es_ES
dc.identifier.e-issn1432-0428-
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderGeneralitat de Catalunyaes_ES
dc.contributor.funderNational Institutes of Health (US)es_ES
dc.contributor.funderDepartment of Agriculture (US)es_ES
dc.contributor.funderNational Institute of Food and Agriculture (US)es_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderCentro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (España)es_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100005825es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100000199es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100000002es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100002809es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.openairetypeartículo-
item.cerifentitytypePublications-
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