Update on male reproductive endocrinology

Abstract

Practitioners of male reproductive and sexual medicine must have an intimate understanding of the physiology of male reproductive endocrinology, as such a knowledge is the cornerstone on which hormonal treatments are based. In this review, we highlight what is known about male reproductive endocrine physiology and the various control mechanisms for the system. We also discuss the limitations of our current understanding of the reproductive physiology. We hope that this review is helpful for male reproductive medicine practitioners in understanding the principles on which hormonal treatments are based.

Testicular Atrophy and Hypothalamic Pathology in COVID-19: Possibility of the Incidence of Male Infertility and HPG Axis Abnormalities

“…While FSH acts on the Sertoli cells, LH targets Leydig cells in the testes leading to the synthesis of testosterone responsible for spermatogenesis [82,83]. As a feedback loop, the circulating concentration of testosterone acts at the hypothalamus to decrease the release of GnRH in order to control the synthesis of FSH and LH in the pituitary [65,84,85]. Local testosterone concentration in the testes is nearly 100 times greater than in the peripheral circulation, and it acts on the Sertoli cells to promote spermatogenesis.…”

Kisspeptin and Testicular Function—Is It Necessary?

“…Optimal spermatogenesis requires the action of both testosterone and FSH. Derangements at any of these steps can cause male infertility [32].…”

CARF promotes spermatogonial self-renewal and proliferation through Wnt signaling pathway

“…We next set out to investigate possible mechanisms underlying the SCO phenotypes observed in the CARFnull mice. Since the hypothalamic-pituitary-gonadal axis (HPG) plays a critical role in spermatogenesis 15 , we first investigated whether the spermatogenic phenotype of CARF KO mice is due to disruption of the endocrine axis. For this, we evaluated the effects of CARF depletion on pituitary, Leydig cell development and seminal vesicles, in all of which we did not observe any apparent phenotypes (data were not shown).…”