Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/105878
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dc.contributor.authorSalvadó, Laiaen
dc.contributor.authorBarroso, Emmaen
dc.contributor.authorGómez-Foix, Anna Mariaen
dc.contributor.authorPalomer, Xavieren
dc.contributor.authorMichalik, Lilianeen
dc.contributor.authorWahli, Walteren
dc.contributor.authorVázquez-Carrera, Manuelen
dc.date.accessioned2014-09-22T06:59:48Zen
dc.date.accessioned2019-12-06T21:59:51Z-
dc.date.available2014-09-22T06:59:48Zen
dc.date.available2019-12-06T21:59:51Z-
dc.date.copyright2014en
dc.date.issued2014en
dc.identifier.citationSalvadó, L., Barroso, E., Gómez-Foix, A. M., Palomer, X., Michalik, L., Wahli, W., et al. (2014). PPARβ/δ prevents endoplasmic reticulum stress-associated inflammation and insulin resistance in skeletal muscle cells through an AMPK-dependent mechanism. Diabetologia, 57(10), 2126-2135.en
dc.identifier.urihttps://hdl.handle.net/10356/105878-
dc.description.abstractAim/hypothesis Endoplasmic reticulum (ER) stress, which is involved in the link between inflammation and insulin resistance, contributes to the development of type 2 diabetes mellitus. In this study, we assessed whether peroxisome proliferator-activated receptor (PPAR)β/δ prevented ER stress-associated inflammation and insulin resistance in skeletal muscle cells. Methods Studies were conducted in mouse C2C12 myotubes, in the human myogenic cell line LHCN-M2 and in skeletal muscle from wild-type and PPARβ/δ-deficient mice and mice exposed to a high-fat diet. Results The PPARβ/δ agonist GW501516 prevented lipid-induced ER stress in mouse and human myotubes and in skeletal muscle of mice fed a high-fat diet. PPARβ/δ activation also prevented thapsigargin- and tunicamycin-induced ER stress in human and murine skeletal muscle cells. In agreement with this, PPARβ/δ activation prevented ER stress-associated inflammation and insulin resistance, and glucose-intolerant PPARβ/δ-deficient mice showed increased phosphorylated levels of inositol-requiring 1 transmembrane kinase/endonuclease-1α in skeletal muscle. Our findings demonstrate that PPARβ/δ activation prevents ER stress through the activation of AMP-activated protein kinase (AMPK), and the subsequent inhibition of extracellular-signal-regulated kinase (ERK)1/2 due to the inhibitory crosstalk between AMPK and ERK1/2, since overexpression of a dominant negative AMPK construct (K45R) reversed the effects attained by PPARβ/δ activation. Conclusions/interpretation Overall, these findings indicate that PPARβ/δ prevents ER stress, inflammation and insulin resistance in skeletal muscle cells by activating AMPK.en
dc.format.extent28 p.en
dc.language.isoenen
dc.relation.ispartofseriesDiabetologiaen
dc.rights© 2014 Springer-Verlag Berlin Heidelberg. This is the author created version of a work that has been peer reviewed and accepted for publication by Diabetologia, Springer-Verlag Berlin Heidelberg. It incorporates referee’s comments but changes resulting from the publishing process, such as copyediting, structural formatting, may not be reflected in this document. The published version is available at: [http://dx.doi.org/10.1007/s00125-014-3331-8].en
dc.subjectDRNTU::Science::Medicineen
dc.titlePPARβ/δ prevents endoplasmic reticulum stress-associated inflammation and insulin resistance in skeletal muscle cells through an AMPK-dependent mechanismen
dc.typeJournal Articleen
dc.contributor.schoolLee Kong Chian School of Medicine (LKCMedicine)en
dc.identifier.doi10.1007/s00125-014-3331-8en
dc.description.versionAccepted versionen
item.grantfulltextopen-
item.fulltextWith Fulltext-
Appears in Collections:LKCMedicine Journal Articles

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