The intervention improved obesity-induced infertility by modulating mitochondrial dynamics, resulting in decreased serum levels of insulin and testosterone, as well as ovarian levels of certain proteins and markers associated with oxidative stress and apoptosis. Additionally, there was an increase in serum estrogen, progesterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH), along with elevated ovarian levels of GnRH receptor (GnRHR), mitofusin2 (Mfn2), mitochondrial transmembrane potential (ΔΨm), and electron transport chain (ETC) complex-I. The gene discussed is INS; the disease is Obesity.