scholarly journals Inhibin is an important factor in the regulation of FSH secretion in the adult male hamster

2000 ◽  
Vol 278 (4) ◽  
pp. E744-E751 ◽  
Author(s):  
Hisashi Kishi ◽  
Mariko Itoh ◽  
Sachiko Wada ◽  
Yoko Yukinari ◽  
Yumiko Tanaka ◽  
...  
Keyword(s):  
Adult Male ◽  
Leydig Cells ◽  
Initial Level ◽  
Plasma Concentrations ◽  
Plasma Testosterone ◽  
Gonadotropin Secretion ◽  
Α Subunit ◽  
Male Golden Hamsters ◽  
Lh Secretion

We investigated the importance of inhibin and testosterone in the regulation of gonadotropin secretion in adult male golden hamsters ( Mesocricetus auratus). After castration, plasma concentrations of inhibin and testosterone were reduced to undetectable, whereas plasma follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were increased. After hemicastration, plasma FSH and LH increased moderately and plasma inhibin decreased to one-half its initial level. Plasma testosterone levels in hemicastrated animals decreased 3 h after hemicastration but returned to those in sham-operated animals at 6 h. Plasma LH in the castrated hamster declined comparably to intact animals with testosterone treatment; plasma FSH also decreased but still remained at levels higher than those in intact animals. After treatment with inhibin in long-term-castrated animals, plasma FSH decreased, whereas plasma LH was not altered. Intact males treated with flutamide, an anti-androgen, showed a significant increase in plasma LH but not in FSH. On the other hand, treatment with anti-inhibin serum induced a significant elevation in plasma FSH, but not in LH. Using immunohistochemistry, we showed that the inhibin α-subunit was localized to both Sertoli and Leydig cells. The present study in adult male hamsters indicates that FSH secretion is regulated mainly by inhibin, presumably from Sertoli and Leydig cells, and that LH secretion is controlled primarily by androgens produced from the Leydig cells. This situation is more similar to that of primates than of rats.

Pituitary and gonadal responses to the long-term pulsatile administration of gonadotrophin-releasing hormone in fetal fetal sheep

1997 ◽  
Vol 153 (3) ◽  
pp. 385-391 ◽  
Author(s):  
G B Thomas ◽  
A N Brooks
Keyword(s):  
Plasma Concentrations ◽  
Reproductive Function ◽  
Inverse Correlation ◽  
Experimental Period ◽  
Immediate Release ◽  
Late Gestation ◽  
Plasma Testosterone ◽  
Fetal Sheep ◽  
Pulsatile Administration

Abstract The fetal hypothalamo–pituitary–gonadal axis reaches a peak in activity at mid-gestation and this is followed by a period of suppression which persists until the onset of puberty. The decline in gonadotrophic activity during late gestation is thought to reflect the maturation of central and peripheral feedback signals. In order to establish if sustained pituitary responsiveness is rate limiting to the reinstatement of reproductive function, we have examined the endocrine consequences of repeated pulsatile GnRH administration to male and fetal sheep during late gestation. Beginning on day 121 of gestation (term=145 days) chronically catheterized fetal sheep were given i.v. pulses of either 500 ng GnRH or saline every 2 h for 14 days. Pituitary and gonadal responses were assessed by measuring changes in plasma concentrations of LH, FSH, inhibin and testosterone (in male fetuses) in response to the first pulse of GnRH on day 1 and to the corresponding pulse on days 4, 7, 10 and 14. In response to the first pulse of GnRH there was an immediate release of LH, with the peak response being significantly (P<0·01) greater than on subsequent days. In male fetuses each pulse of LH was followed by a rise in plasma testosterone concentrations within 40–60 min. The amplitude of these testosterone responses increased significantly (P<0·01) after 9 days of treatment despite a decline in the plasma LH response. Basal FSH concentrations increased progressively (P<0·05) during pituitary stimulation with GnRH in both male and female fetuses. Immunoreactive inhibin concentrations were significantly (P<0·05) higher in males than in females, and there was a gradual increase throughout the experimental period irrespective of treatment. We observed no inverse correlation between inhibin and FSH concentrations. These data show that pulsatile administration of GnRH to fetal sheep during late gestation results in sustained re-activation of pituitary–gonadal function. The decline in fetal gonadotrophins, which is a characteristic feature of late gestation, is therefore likely to result from inadequate GnRH secretion from the fetal hypothalamus rather than an inhibition of pituitary function by peripheral feedback signals. Journal of Endocrinology (1997) 153, 385–391

Testicular oxytocin: effects of intratesticular oxytocin in the rat

1991 ◽  
Vol 130 (2) ◽  
pp. 231-NP ◽  
Author(s):  
H. D. Nicholson ◽  
S. E. F. Guldenaar ◽  
G. J. Boer ◽  
B. T. Pickering
Keyword(s):  
Leydig Cells ◽  
Light And Electron Microscopy ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Epididymal Sperm ◽  
Long Term Effects ◽  
Sperm Counts ◽  
Term Administration

ABSTRACT The long-term effects of oxytocin administration on the testis were studied using intratesticular implants. Adult male rats had an Accurel device containing 20 μg oxytocin (releasing approximately 200 ng/day) implanted into the parenchyma of each testis; control animals received empty devices. The animals were killed at weekly intervals for 4 weeks. Some animals were perfused and the testes processed for light and electron microscopy. Blood was collected from the remaining animals for the measurement of testosterone, dihydrotestosterone, LH, FSH and oxytocin; epididymal sperm counts were measured and the testes were extracted and radioimmunoassayed for testosterone, dihydrotestosterone and oxytocin. Long-term administration of oxytocin resulted in a significant reduction in testicular and plasma testosterone levels throughout the 4-week period examined and, after 14 days of treatment, lipid droplets were seen in the Leydig cells of treated but not control animals. Concentrations of dihydrotestosterone in the plasma and testes of the oxytocin-treated animals, however, were significantly elevated after 7 and 14 days and at no time fell below control values. Plasma FSH levels were also lower in the oxytocin-treated animals. Intratesticular oxytocin treatment did not affect LH or oxytocin concentrations in the plasma, epididymal sperm counts or the number of Leydig cells in the testis. Empty Accurel devices had no effect on testicular morphology. This study provides the first evidence that oxytocin in vivo can modify steroidogenesis in the testis. Journal of Endocrinology (1991) 130, 231–238

scholarly journals Permethrin May Disrupt Testosterone Biosynthesis via Mitochondrial Membrane Damage of Leydig Cells in Adult Male Mouse

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3941-3949 ◽  
Author(s):  
Shu-Yun Zhang ◽  
Yuki Ito ◽  
Osamu Yamanoshita ◽  
Yukie Yanagiba ◽  
Miya Kobayashi ◽  
...  
Keyword(s):  
Adult Male ◽  
Mitochondrial Membrane ◽  
Leydig Cells ◽  
Membrane Damage ◽  
Electron Microscopic Level ◽  
Plasma Testosterone ◽  
Dependent Manner ◽  
Expression Levels ◽  
Testosterone Production ◽  
Testosterone Biosynthesis

Permethrin, a popular synthetic pyrethroid insecticide used to control noxious insects in agriculture, forestry, households, horticulture, and public health throughout the world, poses risks of environmental exposure. Here we evaluate the reproductive toxicity of cis-permethrin in adult male ICR mice that were orally administered cis-permethrin (0, 35, or 70 mg/kg·d) for 6 wk. Caudal epididymal sperm count and sperm motility in the treated groups were statistically reduced in a dose-dependent manner. Testicular testosterone production and plasma testosterone concentration were significantly and dose-dependently decreased with an increase in LH, and a significant regression was observed between testosterone levels and cis-permethrin residues in individual mice testes after exposure. However, no significant changes were observed in body weight, reproductive organ absolute and relative weights, sperm morphology, and plasma FSH concentration after cis-permethrin treatment. Moreover, cis-permethrin exposure significantly diminished the testicular mitochondrial mRNA expression levels of peripheral benzodiazepine receptor (PBR), steroidogenic acute regulatory protein (StAR), and cytochrome P450 side-chain cleavage (P450scc) and enzyme and protein expression levels of StAR and P450scc. At the electron microscopic level, mitochondrial membrane damage was found in Leydig cells of the exposed mouse testis. Our results suggest that the insecticide permethrin may cause mitochondrial membrane impairment in Leydig cells and disrupt testosterone biosynthesis by diminishing the delivery of cholesterol into the mitochondria and decreasing the conversion of cholesterol to pregnenolone in the cells, thus reducing subsequent testosterone production.

Effect of estradiol on the secretion of LH in the GnRH-pretreated rat after treatment with the GnRH-antagonist, Org 30093

1988 ◽  
Vol 119 (4) ◽  
pp. 582-588
Author(s):  
G. A. Schuiling ◽  
N. Valkhof ◽  
T. R. Koiter
Keyword(s):  
Pituitary Gland ◽  
Gnrh Antagonist ◽  
Plasma Concentrations ◽  
Estradiol Benzoate ◽  
The Other ◽  
Gnrh Analogue ◽  
Before And After ◽  
Pituitary Glands ◽  
Lh Secretion

Abstract. LH responses induced in the long-term ovariectomized rat by GnRH or GnRH agonistic analogue are augmented by E2. The augmentation by E2 does not occur during, but after termination of GnRH pretreatment. In this study it was investigated whether the augmenting effect of E2 develops also in the GnRH-pretreated rat when the animals were treated with GnRH antagonistic analogue. Two weeks after ovariectomy rats were treated for 10 days with 250 ng GnRH/h (GnRH-rats), released by sc implanted osmotic minipumps. Control rats received a Silastic 'sham pump'. Rats were simultaneously treated with solvent (oil) or estradiol benzoate (EB, 3 μg, sc). Each group of rats was divided into two subgroups, one receiving solvent, the other the GnRH antagonist, Org 30093 (ANT, 100 μg/injection) on 3 consecutive days. In Experiment 1, the pituitary LH content and the LH secretion following stimulation with the agonistic GnRH analogue buserelin, were measured, in Experiment 2, the plasma concentrations of LH before and after cessation of ANT treatment. The effects of treatment with GnRH, EB and ANT were studied on the basis of 1) the height of the maximal LH response and 2) the halfmaximally effective dose (ed 50) of buserelin. Experiment 1 revealed that GnRH depleted the pitutiary gland to about 42% of its original LH content. In EB-treated GnRH-rats the depletion was even stronger (to 14%). After ANT treatment, the pituitary glands of the GnRH-rats were (partly) repleted (oil: to 65%; EB: to 31%). ANT and EB had no effect on the pituitary LH content in control rats. EB increased the maximal LH response in control rats but not in GnRH-rats. ANT increased the maximal LH response to buserelin in oil-injected control rats as well as in oil- and EB-treated GnRH-rats. In these latter two groups, the increase of the maximal LH response was equally large. However, there was an effect of EB on the ed 50 of buserelin during ANT treatment, the pituitary gland of the EB-treated GnRH-rats had become more sensitive to GnRH. Experiment 2 revealed that GnRH pretreatment reduced the plasma LH concentrations to about 49% of the control levels. EB and ANT, too, lowered the plasma LH concentrations (to about 25%). Neither EB nor ANT, alone or in combination, changed the plasma LH concentrations in GnRH-rats. After cessation of ANT treatment, the plasma LH levels of the oil-injected control rats slowly returned to pretreatment levels, but those of the EB-treated control rats remained suppressed. In the GnRH-rats the reverse was seen: after cessation of ANT treatment, peaks of LH appeared in the plasma of the EB-treated rats, but not in the oil-injected. It is concluded that 1) treatment with ANT is not fully equivalent to termination of GnRH administration because it antagonizes the effects of GnRH only in part: 2) ANT has an intrinsic augmenting effect on the pituitary GnRH-responsiveness, and 3) owing to E2-induced sensitization of the pituitary gland, peaks of LH appear in the plasma of GnRH-rats but not of control rats after termination of ANT treatment.

Reversal of long-term LH deprivation on testosterone secretion and Leydig cell volume, number and proliferation in adult rats

1990 ◽  
Vol 127 (1) ◽  
pp. 47-NP ◽  
Author(s):  
D. S. Keeney ◽  
R. L. Sprando ◽  
B. Robaire ◽  
B. R. Zirkin ◽  
L. L. Ewing
Keyword(s):  
Cell Volume ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Number ◽  
Implant Removal ◽  
Adult Rats ◽  
Testosterone Secretion ◽  
Lh Secretion

ABSTRACT The purpose of this study was to determine whether Leydig cell volume and function could recover fully from long-term LH deprivation upon restoration of endogenous LH secretion, and whether the restoration of LH would elicit a mitogenic response, i.e. stimulate Leydig cell proliferation or affect Leydig cell number per testis. LH secretion was inhibited by treating adult rats with testosterone and oestradiol-filled (TO) silicone elastomer implants (16 weeks), and was restored by removing the implants. Changes in serum concentrations of LH and FSH, LH-stimulated testosterone secretion by testes perfused in vitro, Leydig cell volume and number per testis, average Leydig cell volume and Leydig cell [3H]thymidine incorporation were measured at weekly intervals following implant removal. The TO implants inhibited (P < 0·01) LH secretion, but serum concentrations of FSH were not significantly different (P > 0·10) from control values. After implant removal, serum LH returned to control values within 1 week, whereas serum FSH increased twofold (P < 0·01) and returned to control values at 4 weeks. LH-stimulated in-vitro testosterone secretion was inhibited by more than 99% in TO-implanted rats, but increased (P < 0·01) to 80% of control values by 8 weeks after implant removal. The total volume of Leydig cells per testis and the volume of an average Leydig cell were 14 and 19% of control values respectively, after 16 weeks of TO implantation (P < 0·01), but returned to 83 and 86% of controls (P > 0·10) respectively, by 6 weeks after implant removal. Leydig cell proliferation ([3H]thymidine labelling index) was low (< 0·1%) in both control and TO-implanted rats, increased (P < 0·01) fivefold from 1 to 4 weeks after implant removal and then declined to control values at 6 weeks. The increase in Leydig cell [3H]thymidine incorporation was mimicked by treating TO-implanted rats with exogenous LH, but not FSH. Leydig cells were identified in both the interstitium and the lamina propria of the seminiferous epithelium. The proportion of Leydig cell nuclei in the lamina propria was 30-fold greater (P < 0·01) at 1 and 3 weeks after implant removal (3%) compared with that for control and TO-implanted rats (0·1%). Total Leydig cell number per testis was marginally but not significantly (P = 0·06) decreased in rats treated with TO implants for 16 weeks when compared with controls (18·4±2·2 vs 25·4±1·2 × 106). Three weeks after implant removal, the numbers of Leydig cells per testis were identical (26·8±2·8 × 106) to those in control animals. These results not only demonstrate dramatic morphogenic effects of LH on mature rat Leydig cells, but also suggest that endogenous LH might be mitogenic at least to a subpopulation of Leydig cells. Journal of Endocrinology (1990) 127,47–58

CORRELATION OF PITUITARY AND TESTICULAR RESPONSES TO STIMULATION TESTS IN CRYPTORCHID CHILDREN

1977 ◽  
Vol 86 (3) ◽  
pp. 641-650 ◽  
Author(s):  
Dominique Gendrel ◽  
Marc Roger ◽  
Jean-Louis Chaussain ◽  
Pierre Canlorbe ◽  
Jean-Claude Job
Keyword(s):  
Leydig Cells ◽  
Significant Positive Correlation ◽  
Plasma Testosterone ◽  
Early Puberty ◽  
Testosterone Levels ◽  
Short Course ◽  
Basal Plasma ◽  
Stimulation Tests ◽  
Lh Rh ◽  
Lh Secretion

ABSTRACT LH-RH test and HCG stimulation test were performed in 154 cryptorchid boys aged 1 month to 15 years (64 unilateral and 90 bilateral). Basal plasma LH levels and LH response to LH-RH were significantly lower from infancy to early puberty in cryptorchids compared with controls. Basal FSH levels and FSH response to LH-RH were normal. The post-HCG rise of plasma testosterone was reduced until mid-puberty. A significant positive correlation was found between post-HCG testosterone levels and pre- and post-LH-RH levels of LH. This correlation suggests that testicular maldescent and the decreased ability of Leydig cells to respond to a short course of HCG may result from an early defect or a delay of pituitary LH secretion.

Interactions between nutrition, testosterone and inhibin in the control of gonadotrophin secretion in mature rams

1996 ◽  
Vol 8 (5) ◽  
pp. 855 ◽  
Author(s):  
S Tjondronegoro ◽  
GB Martin ◽  
SR Sutherland ◽  
R Boukhliq
Keyword(s):  
Plasma Concentrations ◽  
Dietary Treatment ◽  
Plasma Testosterone ◽  
Group V ◽  
Intermediate Group ◽  
Gonadotrophin Secretion ◽  
The Mean ◽  
Lh Secretion ◽  
Male Sheep

The role of negative feedback by two testicular hormones, testosterone and inhibin, in the gonadotrophin responses of mature male sheep to changes in nutrition was tested. Six days after castration, 24 Merino rams were assigned to groups that were fed either a diet that maintained their initial liveweight (Intermediate diet), or about half of the Intermediate diet (Low diet), or the Intermediate diet with a supplement of lupin grain (High diet). One week after the change of diet, all animals were given subcutaneous testosterone implants, providing plasma testosterone concentrations of 3.06 +/- 0.14 ng mL-1 (mean +/- s.e.m.; n = 24). The implants were left in place for 7 days, during which time all the rams were also injected subcutaneously with 2 mL steroid-free bovine follicular fluid (bFF) every 8 h, to provide inhibin at mean plasma concentrations of 0.40 +/- 0.04 ng mL-1 (n = 24; compared with 1.50 +/- 0.12 ng mL-1 when the animals were intact). Five days after castration, there were significant increases in the frequency of luteinizing hormone (LH) pulses (from 1.83 +/- 0.23 to 17.3 +/- 0.96 pulses per 12 h; mean +/- s.e.m.; n = 24) and concentrations of FSH (from 0.45 +/- 0.07 to 14.19 +/- 2.7 ng mL-1; n = 24). Dietary treatment did not significantly affect these responses. Treatment with bFF and testosterone for 7 days reduced LH-pulse frequencies and follicle-stimulating hormone (FSH) concentrations in all groups. The degree of reduction was least in the group on the High diet, for which the FSH concentration (6.49 +/- 1.96 ng mL-1) and frequency of LH pulses (7.00 +/- 2.31 pulses per 24 h) were significantly higher than those observed in the other groups. The mean frequency of LH pulses did not differ significantly between the Intermediate group (0.88 +/- 0.61 pulses per 24 h) and the Low group (0.25 +/- 0.25 pulses per 24 h). Similarly, FSH concentrations did not differ significantly between these two groups (1.78 +/- 0.46 for the Intermediate group v. 1.33 +/- 0.26 ng mL-1 for the Low group). It is concluded that there is no response to diet in the absence of testicular hormones and the effects of nutrition on LH secretion in castrated rams given exogenous testosterone and inhibin are similar to those observed in intact rams.

scholarly journals Contrasting effects of different levels of food intake and adiposity on LH secretion and hypothalamic gene expression in sheep

2002 ◽  
Vol 175 (2) ◽  
pp. 383-393 ◽  
Author(s):  
ZA Archer ◽  
SM Rhind ◽  
PA Findlay ◽  
CE Kyle ◽  
L Thomas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Food Intake ◽  
Leptin Receptor ◽  
In Situ Hybridisation ◽  
Plasma Concentrations ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Hypothalamic Arcuate Nucleus ◽  
Lh Secretion

Body reserves (long-term) and food intake (short-term) both contribute nutritional feedback to the hypothalamus. Reproductive neuroendocrine output (GnRH/LH) is stimulated by increased food intake and not by high adiposity in sheep, but it is unknown whether appetite-regulating hypothalamic neurons show this differential response. Castrated male sheep (Scottish Blackface) with oestradiol implants were studied in two 4 week experiments. In Experiment 1, sheep were fed to maintain the initial body condition (BC) score of 2.0+/-0.00 (lower BC (LBC), n=7) or 2.9+/-0.09 (higher BC (HBC), n=9), and liveweight of 43+/-1.1 and 59+/-1.6 kg respectively. LBC and HBC sheep had similar mean plasma LH concentration, pulse frequency and amplitude, but HBC animals had higher mean plasma concentrations of insulin (P<0.01), leptin (P<0.01) and glucose (P<0.01). Gene expression (measured by in situ hybridisation) in the hypothalamic arcuate nucleus (ARC) was higher in LBC than HBC sheep for neuropeptide Y (NPY; 486% of HBC, P<0.01), agouti-related peptide (AGRP; 467%, P<0.05) and leptin receptor (OB-Rb; 141%, P<0.05), but lower for cocaine- and amphetamine-regulated transcript (CART; 92%, P<0.05) and similar between groups for pro-opiomelanocortin (POMC). In Experiment 2, sheep with initial mean BC score 2.4+/-0.03 and liveweight 55+/-0.8 kg were fed a liveweight-maintenance ration (low intake, LI, n=7) while sheep with initial mean BC score 2.0+/-0.03 and liveweight 43+/-1.4 kg were fed freely so that BC score increased to 2.5+/-0.00 and liveweight increased to 54+/-1.4 kg (high intake, HI, n=9). Compared with LI, HI sheep had higher mean plasma LH (P<0.05), baseline LH (P<0.01) and pulse amplitude (P<0.01) and showed a trend towards higher pulse frequency. Although there were no differences in final mean plasma concentrations, there were significant increases over time in mean concentrations of insulin (P<0.001), leptin (P<0.05) and glucose (P<0.001) in HI sheep. Gene expression for AGRP in the ARC was higher in HI than LI animals (453% of LI; P<0.05), but expression levels were similar for NPY, OB-Rb, CART and POMC. Thus, the hypothalamus shows differential responses to steady-state adiposity as opposed to an increase in food intake, in terms of both reproductive neuroendocrine activity and hypothalamic appetite-regulating pathways. Differences in hypothalamic gene expression were largely consistent with contemporary levels of systemic leptin and insulin feedback; however, increased nutritional feedback was stimulatory to GnRH/LH whereas constant high feedback was not. The hypothalamus therefore has the ability to retain a nutritional memory that can influence subsequent responses.

scholarly journals A man with a DAX1/NR0B1 mutation, normal puberty, and an intact hypothalamic–pituitary–gonadal axis but deteriorating oligospermia during long-term follow-up

2013 ◽  
Vol 168 (4) ◽  
pp. K45-K50 ◽  
Author(s):  
Marie-Laure Raffin-Sanson ◽  
Bérénice Oudet ◽  
Sylvie Salenave ◽  
Sylvie Brailly-Tabard ◽  
Martine Pehuet ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Hypogonadotropic Hypogonadism ◽  
Growth Spurt ◽  
Gonadotropin Secretion ◽  
Lh Pulsatility ◽  
Long Term Follow Up ◽  
Human Spermatogenesis ◽  
Lh Secretion

ObjectiveDAX1/NR0B1 mutations cause primary adrenal insufficiency in early childhood and hypogonadotropic hypogonadism (HHG), leading to absent or incomplete sexual maturation. The aim of the study was to prospectively investigate gonadotrope and testicular functions in a patient carrying a DAX1 mutation, who had spontaneous puberty and normal virilization but oligospermia.Case reportThe proband was referred for infertility at the age of 32 years. He reported adrenal insufficiency diagnosed at the age of 19 years. Puberty started at the age of 13 years, with spontaneous virilization, growth spurt, and testicular growth. He reported normal libido and sexual function. Physical examination showed normal virilization, penile length, and testicular volume. However, semen samples showed severe oligospermia. Hormonal measurements confirmed adrenal insufficiency but showed a preserved hypothalamic–pituitary–gonadal axis with normal testosterone and inhibin B; basal and GNRH-stimulated gonadotropin levels and LH pulsatility were also normal. He fathered a first boy by in vitro fertilization and a second boy without medical assistance. As a nephew also had early adrenal insufficiency, the possibility of DAX1 mutation was raised. The same recurrent hemizygous nonsense mutation W39X was found in the proband, his nephew, and in an apparently asymptomatic brother who was found to have adrenal insufficiency, mild HHG, and azoospermia. Several evaluations of the proband over 20 years showed preserved testosterone levels and LH secretion but deteriorating oligospermia.ConclusionLong-term preservation of normal hypothalamic–pituitary–gonadal function in this patient, contrasting with his severe oligospermia, strongly suggests that DAX1 is required for human spermatogenesis, independently of its known role in gonadotropin secretion.

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