The main findings of our present study were that: Firstly, the PPAR-α, PGC-1α, VLCAD expression levels were decreased, while the pAMPK and FAT/CD36 were increased in the canine model of AF; Secondly, metformin increased pAMPK expression in canine model of AF, and prevented the down-regulation of PPAR-α, PGC-1α, VLCAD; Third, metformin prevented the atrial metabolic remolding of AF partly through the AMPK/PPAR-α/VLCADS pathway. This evidence concerns the gene PRKAA1 and atrial fibrillation.