In this context, an obesity-associated increase in leptin may influence reproductive function through various mechanisms, such as an inhibitory effect on the kisspeptin–GnRH pathway [107], an altered nutritional support of germ cells due to the impaired metabolism of Sertoli cells that express leptin-receptors [108], an impaired testosterone production in Leydig cells, and an increased oxidative stress with mitochondrial dysfunction in spermatozoa [102]. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.