Role of FSH in the Control of Testicular Function

Abstract

Follicle stimulating hormone (FSH) binds to the plasma membranes of Sertoli cells and, apparently, spermatogonia; the hormone may then be taken into the cytoplasm of its target cells and metabolized there. In the immature testis, binding of FSH to Sertoli cells leads to activation of adenylate cyclase, formation of cyclic AMP (CAMP), and activation of a CAMP-dependent protein kinase. There is a subsequent increase in the rates of RNA, protein, and DNA synthesis. Normal adult testis is unresponsive to FSH, one reason being the destruction of CAMP by a phosphodiesterase. After hypophysectomy of adult animals this enzyme disappears and FSH is again able to stimulate RNA and protein synthesis. Other factors contributing to the insensitivity of the mature testis are an FSH binding inhibitor, a protein kinase inhibitor, and inactivation of FSH.FSH increases the formation by Sertoli cells of structural proteins and an androgen-binding protein (ABP) that the Sertoli cells secrete into the extracellular fluid surrounding the cells of the germinal epithelium. It is thought that ABP buffers fluctuations in the concentration of androgen in the extracellular fluid of the germinal epithelium as well as transporting androgen to the lumen of the epididymis.In immature animals FSH increases the number of Sertoli cells, which accounts for the testicular hypertrophy that follows hemicastration. FSH is responsible for maturational changes in immature Sertoli cells and for morphological changes associated with in vitro aggregation of Sertoli cells to form colonies. FSH-induced changes in the shape of Sertoli cells are mediated by a calcium-dependent regulator protein, calmodulin. FSH also stimulates the Sertoli cells to secrete a plasminogen activator whose role is not known.FSH has effects on testicular germ cells in immature animals and during the restoration of spermatogenesis in adults, but it is not known whether the Sertoli cells mediate its actions on the germ cells, though this would seem likely. Administration of FSH to immature rats and mice increases the number of spermatogonia by reducing the proportion that degenerate. This may be due to a stimulatory effect of the hormone on DNA synthesis. Androgen and FSH appear to act synergistically to stimulate accumulation of primary spermatocytes and formation of spermatids in immature rats. During the restoration of spermatogenesis in adult rats and mice FSH also acts synergistically with androgen, increasing the proportions of cells passing through meiosis and spermiogenesis. Immunization experiments suggest that FSH is needed for the formation of normal numbers of spermatocytes and spermatids in immature animals, but studies in adults have given conflicting results.FSH appears to influence development of the interstitial tissue, particularly by inducing luteinizing hormone (LH) receptors on Leydig cells. The presence of some LH may be necessary for FSH to have this effect. FSH can stimulate a number of steroid transformations, such as conversion of testosterone to dihydrotesto...

Effect of human menopausal gonadotropin on testicular morphometry, gonadal and extragonadal sperm reserves of rabbit bucks

“…Sertoli cells are known to be responsible for nurturing the developing spermatids and on Leydig cells to produce androgenic hormones which enhance male reproductive traits. The results herein further confirmed the report of Davies (1981) that the administration of gonadotrophin to immature rats and mice increases the number of spermatogonia by reducing the proportion that degenerate. This may be due to a stimulatory effect of the hormone on DNA synthesis of the sperm cells.…”

“…This may be due to a stimulatory effect of the hormone on DNA synthesis of the sperm cells. Furthermore, gonadotrophin also increases the proportion of cells passing through meiosis and spermatogenesis (Davies, 1981;Haywood et al, 2003;Matthiesson et al, 2006) Means bearing different letters of superscript within the same row differ significantly (P<0.05). Orgebin-Crist (1968).…”

Effect of Vitamin D Deficiency on Testicular Function in the Rat

“…Early primary spermatocytes move across the barrier, and further germ cell development occurs in the adluminal compartment where Sertoli cells control the composition of the fluid which surrounds the germ cells by secret ing pyruvate and lactate which may support the synthetic activities and survival of germ cells, and they concluded that there is a close functional relationship between Sertoli cells and germ cells [21,22], Rivarola et al [23] proposed that Sertoli cells stimulate the syn thesis of RNA and DNA in spermatogenic cells. The Lcydig cell function may also be modified by Sertoli cells [25]. These observa tions and an already reported [9] decrease in the testosterone level in vitamin-D-deficient rats support our observation of decreased Leydig cell count of the present study.…”

Effect of Vitamin D Repletion on Testicular Function in Vitamin D-Def icient Rats

“…The role of Sertoli cells and Leydig cells on the maturation of spermatozoa is known [13][14][15][16]. The Sertoli cells modify the Leydig cell function as well [17], The reversed GTP activity which is a marker of Sertoli cell func tion and return of the number of Leydig cells towards normal (table 1) may be responsible for the increased spermatogenesis seen in this study at lower doses of vitamin D administra tion.…”