AMPK emerges as a key mediator in the dysregulation and highlights its potential as a therapeutic target to mitigate the adverse effects of obesity on mitochondrial biogenesis and mtDNA heteroplasmy, oocyte maturation and quality, offering promising avenues to improve reproductive and health outcomes of both mothers and their offspring. This evidence concerns the gene PRKAA1 and obesity due to melanocortin 4 receptor deficiency.