Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/153809
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dc.contributor.authorAguilar-Recarte, Daviden_US
dc.contributor.authorBarroso, Emmaen_US
dc.contributor.authorGumà, Annaen_US
dc.contributor.authorPizarro-Delgado, Javieren_US
dc.contributor.authorPeña, Lucíaen_US
dc.contributor.authorRuart, Mariaen_US
dc.contributor.authorPalomer, Xavieren_US
dc.contributor.authorWahli, Walteren_US
dc.contributor.authorVázquez-Carrera, Manuelen_US
dc.date.accessioned2021-12-14T08:25:06Z-
dc.date.available2021-12-14T08:25:06Z-
dc.date.issued2021-
dc.identifier.citationAguilar-Recarte, D., Barroso, E., Gumà, A., Pizarro-Delgado, J., Peña, L., Ruart, M., Palomer, X., Wahli, W. & Vázquez-Carrera, M. (2021). GDF15 mediates the metabolic effects of PPARβ/δ by activating AMPK. Cell Reports, 36(6), 109501-. https://dx.doi.org/10.1016/j.celrep.2021.109501en_US
dc.identifier.issn2211-1247en_US
dc.identifier.urihttps://hdl.handle.net/10356/153809-
dc.description.abstractPeroxisome proliferator-activated receptor β/δ (PPARβ/δ) activates AMP-activated protein kinase (AMPK) and plays a crucial role in glucose and lipid metabolism. Here, we examine whether PPARβ/δ activation effects depend on growth differentiation factor 15 (GDF15), a stress response cytokine that regulates energy metabolism. Pharmacological PPARβ/δ activation increases GDF15 levels and ameliorates glucose intolerance, fatty acid oxidation, endoplasmic reticulum stress, and inflammation, and activates AMPK in HFD-fed mice, whereas these effects are abrogated by the injection of a GDF15 neutralizing antibody and in Gdf15-/- mice. The AMPK-p53 pathway is involved in the PPARβ/δ-mediated increase in GDF15, which in turn activates again AMPK. Consistently, Gdf15-/- mice show reduced AMPK activation in skeletal muscle, whereas GDF15 administration results in AMPK activation in this organ. Collectively, these data reveal a mechanism by which PPARβ/δ activation increases GDF15 levels via AMPK and p53, which in turn mediates the metabolic effects of PPARβ/δ by sustaining AMPK activation.en_US
dc.language.isoenen_US
dc.relation.ispartofCell Reportsen_US
dc.rights© 2021 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).en_US
dc.subjectScience::Medicineen_US
dc.titleGDF15 mediates the metabolic effects of PPARβ/δ by activating AMPKen_US
dc.typeJournal Articleen
dc.contributor.schoolLee Kong Chian School of Medicine (LKCMedicine)en_US
dc.identifier.doi10.1016/j.celrep.2021.109501-
dc.description.versionPublished versionen_US
dc.identifier.pmid34380027-
dc.identifier.scopus2-s2.0-85112150186-
dc.identifier.issue6en_US
dc.identifier.volume36en_US
dc.identifier.spage109501en_US
dc.subject.keywordsGrowth Differentiation Factor 15en_US
dc.subject.keywordsPPARβ/δen_US
dc.description.acknowledgementThis study was partly supported by grants from the Spanish Ministry of Economy and Competitiveness (SAF2015-64146- R and RTI2018-093999-B-100) and European Union ERDF funds.en_US
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