Endocrine control of spermatogenesis: Role of FSH and LH/ testosterone

Abstract

Evaluation of testicular functions (production of sperm and androgens) is an important aspect of preclinical safety assessment and testicular toxicity is comparatively far more common than ovarian toxicity. This chapter focuses (1) on the histological sequelae of disturbed reproductive endocrinology in rat, dog and nonhuman primates and (2) provides a review of our current understanding of the roles of gonadotropins and androgens. The response of the rodent testis to endocrine disturbances is clearly different from that of dog and primates with different germ cell types and spermatogenic stages being affected initially and also that the end-stage spermatogenic involution is more pronounced in dog and primates compared to rodents. Luteinizing hormone (LH)/testosterone and follicle-stimulating hormone (FSH) are the pivotal endocrine factors controlling testicular functions. The relative importance of either hormone is somewhat different between rodents and primates. Generally, however, both LH/testosterone and FSH are necessary for quantitatively normal spermatogenesis, at least in non-seasonal species.

Quantitative and cytological studies of interstitial (Leydig) cells in the scrotal and retained testes of unilateral cryptorchid West African Dwarf goats

“…It is well established that testosterone is produced by interstitial cells (Shima et al, 2013a,b) and is essential for maintaining and stimulating normal spermatogenesis (Baker and O'Shaughnessy, 2001;Ramaswamy and Weinbauer, 2015). Bergh and Damber (1978) in a morphometric and functional investigation of the interstitial cells of experimental cryptorchidism in rats observed that interstitial cell function in the cryptorchid testis was maintained at 30 days but highly impaired at 100 days of age.…”

Obesity, a serious etiologic factor for male subfertility in modern society

“…Additionally, FSH is another important regulator of Sertoli cells, stimulating virtually all functions related to spermatogenesis. Therefore, the low testosterone and FSH levels in obese men can be a cause for impaired spermatogenesis and finally lead to reduced sperm counts and subfertility (Cheng et al 2010, Ramaswamy & Weinbauer 2015.…”

Loss of microRNA-7a2 induces hypogonadotropic hypogonadism and infertility

“…This action regulates synthesis and release of both gonadotropins, LH and FSH, that control gonadal maturation and adult reproductive physiology via stimulation of sex steroid synthesis (1). In males, FSH stimulates proliferation of immature Sertoli cells and spermatogonia, whereas LH stimulates Leydig cells to produce testosterone (4). In females, LH triggers ovulation, promotes development of the corpus luteum, and stimulates theca cells to produce androgens, whereas FSH stimulates recruitment of secondary ovarian follicles and the secretion of estradiol from granulosa cells, thereby promoting follicular maturation, which ultimately leads to ovulation (5).…”