236. Effects of long term recombinant rat follicle-stimulating hormone replacement on the restoration of spermatogenesis after chronic suppression of gonadotrophins in adult rats

2008 ◽  
Vol 20 (9) ◽  
pp. 36
Author(s):  
S. M. Ruwanpura ◽  
P. G. Stanton ◽  
D. M. Robertson ◽  
R. I. McLachlan ◽  
Y. Makanji ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Germ Cells ◽  
Follicle Stimulating Hormone ◽  
Inhibin B ◽  
Testis Weight ◽  
Adult Rats ◽  
Early Pachytene ◽  
Pachytene Spermatocytes ◽  
Stimulating Hormone

Follicle stimulating hormone (FSH) in short-term rat studies supports spermatogenesis at multiple levels, notably spermatogonial development. The role of FSH in supporting full spermatogenesis in rats is still in question as long-term studies have not been possible due the development of neutralising antibodies to heterologous FSH preparations. This study sought to assess the effects of a homologous recombinant rat FSH (rr-FSH) preparation on the long-term restoration of spermatogenesis. Adult rats were GnRH-immunised (GnRH-im) for 12 weeks then, administered an anti-androgen; flutamide (flut), alone or together with rr-FSH (8µg/rat/daily) for 56 days (1 spermatogenic cycle). Germ and Sertoli cell numbers were quantified using an optical disector stereological method. Testis weight, serum FSH and inhibin B and Sertoli cell nuclear volume were significantly reduced to 15%, 13%, 25% and 57% of controls respectively, following GnRH-im+flut treatment. GnRH-im+flut treatment reduced A/I spermatogonial, type B spermatogonial+preleptotene, leptotene+zygotene and early pachytene spermatocyte numbers to 28%, 68%, 50% and 19% (P < 0.001) of controls respectively, with later germ cells rarely observed. After FSH treatment, no significant affect on testis weight, serum FSH and inhibin B or Sertoli cell number were observed. However, rr-FSH treatment significantly increased numbers of A/I spermatogonia, leptotene+zygotene and early pachytene spermatocytes from 28 = >42%, 50 = >69% and 19 = >27% of controls, respectively, while no differences were observed in later germ cell types. rr-FSH also increased (P < 0.05) the volume of Sertoli cell nuclei from 57 = >66% of control. In conclusion, FSH is unable to support full rat spermatogenesis; however, FSH can partially support germ cells notably spermatogonia through to early pachytene spermatocytes, despite the absence of androgenic support.

scholarly journals Male Central Hypogonadism in Paediatrics – the Relevance of Follicle-stimulating Hormone and Sertoli Cell Markers

2018 ◽  
Vol 14 (2) ◽  
pp. 67 ◽  
Author(s):  
Romina P Grinspon ◽  
Mariela Urrutia ◽  
Rodolfo A Rey
Keyword(s):  
Sertoli Cell ◽  
Physiological State ◽  
Pubertal Development ◽  
Follicle Stimulating Hormone ◽  
Early Infancy ◽  
Inhibin B ◽  
Clear Understanding ◽  
Male Hypogonadism ◽  
Cell Markers ◽  
Stimulating Hormone

The definition of male hypogonadism, used in adult endocrinology, is not fully applicable to paediatrics. A clear understanding of the developmental physiology of the hypothalamic-pituitary-testicular axis is essential for the comprehension of the pathogenesis of hypogonadal states in boys and for the establishment of adequate definitions and classifications in paediatric ages. This is particularly true for central hypogonadism, usually called hypogonadotropic in adults. Because childhood is a period characterised by a physiological state of low gonadotropin and testosterone production, these markers of hypogonadism, typically used in adult endocrinology, are uninformative in the child. This review is focused on the physiological importance of prepubertal Sertoli cell markers – anti-Müllerian hormone (AMH) and inhibin B – and of the intratesticular actions of follicle-stimulating hormone (FSH) and testosterone during early infancy and the first stages of pubertal development. We discuss the role of FSH in regulating the proliferation of Sertoli cells – the main determinant of prepubertal testicular volume – and the secretion of AMH and inhibin B. We also address how intratesticular testosterone concentrations have different effects on the seminiferous tubule function in early infancy and during pubertal development.

CHRONIC MEDIAN EMINENCE LESIONS AND OVARIECTOMY: EFFECTS ON FOLLICLE-STIMULATING HORMONE SECRETION IN THE RAT

1971 ◽  
Vol 51 (4) ◽  
pp. 665-674 ◽  
Author(s):  
E. B. CRAMER ◽  
R. E. TRAUM ◽  
S. A. D'ANGELO
Keyword(s):  
Median Eminence ◽  
Follicle Stimulating Hormone ◽  
Hormone Secretion ◽  
Serum Levels ◽  
Ovariectomized Rats ◽  
Adult Rats ◽  
Serum Hormone ◽  
Marked Atrophy ◽  
Stimulating Hormone

SUMMARY Pituitary and serum follicle-stimulating hormone (FSH) concentrations were determined by the Steelman—Pohley ovarian augmentation bioassay method in normal adult rats and in rats subjected to ovariectomy and/or electrolytic lesioning of the tuberal hypothalamus 10, 30 or 90 days previously. Ovariectomy resulted in a rapid, significant increase in FSH concentration of the adenohypophysis. Pituitary FSH concentrations were increased sixfold 10 and 30 days after ovariectomy and by 90 days were increased by 700%. (Hormone stores in the adenohypophysis increased correspondingly.) Serum FSH levels in ovariectomized rats also increased but at a slower rate. Ten days after ovariectomy, serum FSH levels were still normal. Thirty and ninety days postoperatively, serum FSH titres were doubled and quintupled, respectively. Chronic median eminence lesions eventually caused obesity, a marked atrophy of the reproductive system and significant increase in the FSH concentration of the adenohypophysis. Follicle-stimulating hormone was not detected in the sera of rats with short-term lesions but serum hormone levels were in the normal range 30 and 90 days after the lesions were made. Complete destruction of the median eminence in ovariectomized rats was associated with further increase in pituitary FSH concentration and content. Ninety days after simultaneous lesioning and ovariectomy, FSH concentration of the adenohypophysis was almost twice that of the ovariectomized control and the hormone content was about 14 times that in the normal pituitary. In contrast, the raised FSH serum levels observed after long-term ovariectomy were significantly reduced (50%). It is concluded that chronic median eminence lesions which induce obesity and ovarian atrophy in rats differentially affect synthesis and release of FSH by the adenohypophysis.

INFLUENCE OF GERM CELLS UPON TRANSFERRIN SECRETION BY RAT SERTOLI CELLS in vitro

1988 ◽  
Vol 118 (3) ◽  
pp. R13-R16 ◽  
Author(s):  
B. LE MAGUERESSE ◽  
C. PINEAU ◽  
F. GUILLOU ◽  
B. JEGOU
Keyword(s):  
Sertoli Cell ◽  
Cell Cultures ◽  
Germ Cells ◽  
Sertoli Cells ◽  
Seminiferous Tubules ◽  
Adult Rats ◽  
Hypotonic Treatment ◽  
Old Rats ◽  
Pachytene Spermatocytes

ABSTRACT Indirect approach (hypotonic treatment) and direct approaches (co-cultures and conditioned media) were used in order to investigate the effects of germ cells from adult rats upon transferrin secretion by Sertoli cell cultures prepared from 20-day-old rats. Removal of germ cells contaminating the Sertoli cell cultures resulted in a significant decrease in transferrin secretion whereas the addition of crude germ cell preparations or of enriched preparations of pachytene spermatocytes, early spermatids and of liver epithelial cells (LEC) markedly stimulated this parameter. Furthermore, spent media of pachytene spermatocytes and of early spermatids, but not of LEC, also stimulated transferrin production. It is concluded that germ cells normally located within the adluminal compartment of the seminiferous tubules may be capable of controlling their own supply of iron via their influence upon transferrin secretion by the Sertoli cells.

scholarly journals FSH and testosterone signaling in Sertoli cells

Reproduction ◽  
2005 ◽  
Vol 130 (1) ◽  
pp. 15-28 ◽  
Author(s):  
William H Walker ◽  
Jing Cheng
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Signaling Pathways ◽  
Sertoli Cell ◽  
Germ Cells ◽  
Sertoli Cells ◽  
Follicle Stimulating Hormone ◽  
Reproductive Potential ◽  
Recent Advances ◽  
Stimulating Hormone

Testosterone and follicle-stimulating hormone (FSH) are required to obtain full reproductive potential. In the testis, somatic Sertoli cells transduce signals from testosterone and FSH into the production of factors that are required by germ cells as they mature into spermatozoa. Recent advances in identifying new signaling pathways that are regulated by FSH and testosterone have allowed for refinement in the understanding of the independent, overlapping and synergistic actions of these hormones. In this review, we discuss the signaling pathways that are regulated by FSH and testosterone as well as the resulting metabolic and gene expression changes that occur as related to Sertoli cell proliferation, differentiation and the support of spermatogenesis.

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