The underlying mechanisms of the anti-obesity of hAMSCs-CM might be involved in inhibiting PPARγ and C/EBPα-mediated lipid synthesis and adipogenesis, promoting GLUT4-mediated glucose metabolism, elevating UCP1/PPARα/PGC1α-mediated energy expenditure, and enhancing STAT3-ARG1-mediated M2-type macrophage polarization during the development of obesity. The gene discussed is PPARGC1A; the disease is obesity due to melanocortin 4 receptor deficiency.