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PGC1α , a transcriptional coactivator, interacts with PPARs and others to regulate skeletal muscle metabolism.  PGC1α  undergoes splicing to produce several mRNA variants, with the  NTPGC1α  variant having a similar biological function to the full length  PGC1α  ( FLPGC1α ). CVD is associated with obesity and T2D and a lower percentage of type 1 oxidative fibers and impaired mitochondrial function in skeletal muscle, characteristics determined by  PGC1α  expression.  PGC1α  expression is epigenetically regulated in skeletal muscle to determine mitochondrial adaptations, and epigenetic modifications may regulate mRNA splicing. We report in this paper that skeletal muscle  PGC1α   −1 nucleosome (−1N) position is associated with splice variant  NTPGC1α  but not  FLPGC1α  expression. Division of participants based on the −1N position revealed that those individuals with a −1N phased further upstream from the transcriptional start site (UP) expressed lower levels of  NTPGC1α  than those with the −1N more proximal to TSS (DN). UP showed an increase in body fat percentage and serum total and LDL cholesterol. These findings suggest that the −1N may be a potential epigenetic regulator of  NTPGC1α  splice variant expression, and −1N position and  NTPGC1α  variant expression in skeletal muscle are linked to CVD risk. This trial is registered with clinicaltrials.gov, identifier  NCT00458133 .

PGC1α−1 Nucleosome Position and Splice Variant Expression and Cardiovascular Disease Risk in Overweight and Obese Individuals