Abstract：
:Cellular metabolite balance and mitochondrial function are under circadian control, but the pathways connecting the molecular clock to these functions are unclear. Peroxisome proliferator-activated receptor delta (PPARδ) enables preferential utilization of lipids as fuel during exercise and is a major driver of exercise endurance. We show here that the circadian repressors CRY1 and CRY2 function as co-repressors for PPARδ. Cry1-/-;Cry2-/- myotubes and muscles exhibit elevated expression of PPARδ target genes, particularly in the context of exercise. Notably, CRY1/2 seem to repress a distinct subset of PPARδ target genes in muscle compared to the co-repressor NCOR1. In vivo, genetic disruption of Cry1 and Cry2 enhances sprint exercise performance in mice. Collectively, our data demonstrate that CRY1 and CRY2 modulate exercise physiology by altering the activity of several transcription factors, including CLOCK/BMAL1 and PPARδ, and thereby alter energy storage and substrate selection for energy production.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Jordan SD,Kriebs A,Vaughan M,Duglan D,Fan W,Henriksson E,Huber AL,Papp SJ,Nguyen M,Afetian M,Downes M,Yu RT,Kralli A,Evans RM,Lamia KAdoi
10.1016/j.cmet.2017.06.002subject
Has Abstractpub_date
2017-07-05 00:00:00pages
243-255.e6issue
1eissn
1550-4131issn
1932-7420pii
S1550-4131(17)30344-3journal_volume
26pub_type
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