Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.cmet.2017.04.006
Title: PPARδ Promotes Running Endurance by Preserving Glucose
Authors: Fan, 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
Keywords: Science & Technology
Life Sciences & Biomedicine
Cell Biology
Endocrinology & Metabolism
ACTIVATED-RECEPTOR-DELTA
SKELETAL-MUSCLE
EXERCISE MIMETICS
RNA-SEQ
METABOLISM
EXPRESSION
ADAPTATION
OXIDATION
INCREASE
OBESITY
Issue Date: 2-May-2017
Publisher: CELL PRESS
Citation: Fan, 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
Abstract: Management 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.
Source Title: CELL METABOLISM
URI: https://scholarbank.nus.edu.sg/handle/10635/247832
ISSN: 1550-4131
1932-7420
DOI: 10.1016/j.cmet.2017.04.006
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