Kisspeptin and its effect on mammalian spermatogensis.

Kisspeptin and its receptor, GPR54, are regarded as key regulators of and catalysts for male puberty onset, and also fundamental gatekeepers of spermatogenesis in mammals. Consequently, the loss function of kisspeptin or GPR54 leads to a symptom of hypogonadotropic hypogonadism (HH) in human and HH accompanied by lower gonadotrophic hormone levels, smaller testes, impaired spermatogenesis and abnormal sexual maturation in mice. Besides its well- recognized functions in hypothalamus before and during puberty, accumulating data strongly support kisspeptin production in tests, and participation in somatic and germ cell development and sperm functions as well. This review summarizes the published data from animal models and humans in in vivo and in vitro studies regarding the testicular activity of kisspeptins to conserve male fertility. Kisspeptin might be a new potential therapeutic target for the treatment of male fertility defects and disorders.