AMPK does not play a requisite role in regulation of PPARGC1A gene expression via the alternative promoter in endurance-trained human skeletal muscle

In human skeletal muscle, PGC-1α is constitutively expressed via the canonical promoter. By contrast, the expression of PGC-1α mRNA via the alternative promoter was found to be highly dependent on the intensity of exercise and to contribute largely to the post-exercise increase of total PGC-1α mRNA. This study investigated the role of AMPK in regulating PGC-1α gene expression via the alternative promoter through a cAMP responsive element-binding protein-1 (CREB1)-dependent mechanism in human skeletal muscle. AMPK activation and PGC-1α gene expression were assayed in skeletal muscle of nine endurance-trained men before and after low-intensity exercise (38% of VО_2max), and with or without administration of a single dose (2 g) of the AMPK activator metformin. Low-intensity exercise markedly and significantly increased (∼100-fold, P < 0.05) the expression of PGC-1α mRNA via the alternative promoter, without increasing ACC^Ser79/222 (a marker of AMPK activation) and AMPK^Thr172 phosphorylation. Moreover, in contrast to placebo, metformin increased the level of ACC^Ser79/222 phosphorylation immediately after exercise (2.6-fold, P < 0.05). By contrast, post-exercise expression of PGC-1α gene via the alternative promoter was not affected. This study was unable to confirm that AMPK plays a role in regulating PGC-1α gene expression via the alternative promoter in endurance-trained human skeletal muscle.

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