Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.cmet.2017.04.006
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dc.titlePPARδ Promotes Running Endurance by Preserving Glucose
dc.contributor.authorFan, Weiwei
dc.contributor.authorWaizenegger, Wanda
dc.contributor.authorLin, Chun Shi
dc.contributor.authorSorrentino, Vincenzo
dc.contributor.authorHe, Ming-Xiao
dc.contributor.authorWall, Christopher E
dc.contributor.authorLi, Hao
dc.contributor.authorLiddle, Christopher
dc.contributor.authorYu, Ruth T
dc.contributor.authorAtkins, Annette R
dc.contributor.authorAuwerx, Johan
dc.contributor.authorDownes, Michael
dc.contributor.authorEvans, Ronald M
dc.date.accessioned2024-04-11T03:48:33Z
dc.date.available2024-04-11T03:48:33Z
dc.date.issued2017-05-02
dc.identifier.citationFan, Weiwei, Waizenegger, Wanda, Lin, Chun Shi, Sorrentino, Vincenzo, He, Ming-Xiao, Wall, Christopher E, Li, Hao, Liddle, Christopher, Yu, Ruth T, Atkins, Annette R, Auwerx, Johan, Downes, Michael, Evans, Ronald M (2017-05-02). PPARδ Promotes Running Endurance by Preserving Glucose. CELL METABOLISM 25 (5) : 1186-1193. ScholarBank@NUS Repository. https://doi.org/10.1016/j.cmet.2017.04.006
dc.identifier.issn1550-4131
dc.identifier.issn1932-7420
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/247832
dc.description.abstractManagement of energy stores is critical during endurance exercise; a shift in substrate utilization from glucose toward fat is a hallmark of trained muscle. Here we show that this key metabolic adaptation is both dependent on muscle PPARδ and stimulated by PPARδ ligand. Furthermore, we find that muscle PPARδ expression positively correlates with endurance performance in BXD mouse reference populations. In addition to stimulating fatty acid metabolism in sedentary mice, PPARδ activation potently suppresses glucose catabolism and does so without affecting either muscle fiber type or mitochondrial content. By preserving systemic glucose levels, PPARδ acts to delay the onset of hypoglycemia and extends running time by ∼100 min in treated mice. Collectively, these results identify a bifurcated PPARδ program that underlies glucose sparing and highlight the potential of PPARδ-targeted exercise mimetics in the treatment of metabolic disease, dystrophies, and, unavoidably, the enhancement of athletic performance.
dc.language.isoen
dc.publisherCELL PRESS
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectCell Biology
dc.subjectEndocrinology & Metabolism
dc.subjectACTIVATED-RECEPTOR-DELTA
dc.subjectSKELETAL-MUSCLE
dc.subjectEXERCISE MIMETICS
dc.subjectRNA-SEQ
dc.subjectMETABOLISM
dc.subjectEXPRESSION
dc.subjectADAPTATION
dc.subjectOXIDATION
dc.subjectINCREASE
dc.subjectOBESITY
dc.typeArticle
dc.date.updated2024-04-08T10:33:37Z
dc.contributor.departmentBIOCHEMISTRY
dc.description.doi10.1016/j.cmet.2017.04.006
dc.description.sourcetitleCELL METABOLISM
dc.description.volume25
dc.description.issue5
dc.description.page1186-1193
dc.published.statePublished
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