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Porcine steroidogenic factor-1 gene (pSF-1) expression and analysis of embryonic pig gonads during sexual differentiation.

The porcine steroidogenic factor-1 gene (pSF-1) was cloned using a combination of genomic and RT-PCR based cloning methods. pSF-1 consists of an open reading frame of 1383 nt corresponding to a deduced amino acid sequence of 461 aa, similar to bovine and human SF-1. Sequence homologies between pSF-1 and human, bovine and mouse molecules indicate strong evolutionary conservation at both the nt and aa levels. Northern analysis of pSF-1 expression in adult steroidogenic tissues correlated with porcine steroidogenic acute regulatory protein gene (pStAR) and porcine side chain cleavage (pP450scc) gene expression. Notably, pSF-1 expression was readily detected in neonatal testes, absent at 3 weeks of age, and again readily detected at 3 months and in adult testes. pSF-1 expression was weak but detectable in placental tissues at various times of gestation, and was correlated with pStAR and pP450scc expression, indicating classical steroidogenesis in this organ. In developing gonads from 6-12 weeks of gestation, i.e. during the time of sex differentiation in the pig, Northern analysis demonstrated increasing expression of PSF-1 in fetal testes and no expression in ovaries. This expression pattern was paralleled for pStAR, pP450scc, and porcine Müllerian inhibitory substance (pMIS), consistent with pSF-1 involvement in both steroid and protein hormone secretions of the developing testes during sex differentiation. Porcine SRY HMG-box related gene-9 (pSOX-9) expression also paralleled that of pSF-1 in developing testes. In contrast, DSS-AHC critical region on the X chromosome, gene 1 (pDAX-1) was expressed predominantly in the developing ovaries, indicating a possible reciprocal regulation of pSF-1 and pDAX-1 genes in developing pig testes and ovaries.

Amino Acid Sequence↗

Hormonal regulation of proliferation of granulosa and Leydig cell lines derived from gonadal tumors of transgenic mice expressing the inhibin-alpha subunit promoter/simian virus 40 T-antigen fusion gene.

We have produced a transgenic (TG) mouse model expressing the Simian Virus 40 T-antigen (Tag) gene, driven by a 6-kb fragment of the mouse inhibin-alpha subunit promoter (inh-alpha). The mice develop gonadal tumors with 100% penetrance by the age of 5-8 months, of granulosa cell origin in the ovary, and of Leydig cell origin in the testis. In the present study, we characterized the hormonal regulation of proliferation of two immortalized cell lines, BLT-1, originating from a Leydig cell tumor, and NT-1, originating from a granulosa cell tumor. [3H]-thymidine incorporation in both types of cells was stimulated by activin (> or = 10-30 microg/l), while inhibin had no effect. Transforming growth factor (TGF)-beta, at > or = 0.01 microg/l, stimulated proliferation of the granulosa tumor cells, but no effect was found on the Leydig tumor cells. Progesterone inhibited the proliferation of both cell lines, although the granulosa tumor cells were clearly less sensitive than the Leydig cells to this effect ( > or = 3 micromol/l vs. > 10 nmol/l, respectively). hCG had no effect on the Leydig tumor cell DNA synthesis whereas at high concentration (100 microg/l) it stimulated that of the granulosa cells. We also investigated in BLT-1 and NT-1 cells whether the proliferative changes were related to concomitant changes in Tag expression. In BLT-1 cells, this was stimulated by activin, progesterone and hCG, even though the latter substance did not affect cell proliferation. In contrast, TGF-beta inhibited Tag expression. In NT-1 cells, the expression of Tag was stimulated by activin, while hCG had no effect. In contrast, it was reduced by progesterone, inhibin and TGF-beta. In conclusion, our results indicate that the granulosa and Leydig tumor cells, despite similar mechanism of immortalization, respond differently to several mitotic stimuli. The responses in the level of Tag expression in these cells did not always correlate with the changes observed in cell proliferation, indicating the independence of these two phenomena.

Activins↗

Somatic condition of the fish, Notopterus notopterus (Pallas) during different phases of the reproductive cycle.

The study on the mathematical relationship between length and weight of fishes has considerable importance in fishery research especially for the study of fish population dynamics and patterns of growth in fish stocks. This aspect is useful in rationally managing the population of fishes, and is an index of relative robustness of the fish). Variations from expected weight or length of an individual fish or group of fish indicate the general well being and state of gonadal development. The condition of fish can be influenced by the onset of maturity. The results indicate that the overall condition of the female and male fish seems to get improved towards the approach of maturing and mature stages of the gonads during pre-spawning phases. The reduction in the condition factor (K) and somatic condition factor (Ks) during spawning phase may be because of the fish becoming exhausted due to spawning activity. Although improvement in the condition of the fish was observed on the approach of breeding period, the overall condition seems to be better in the aquatic body from which the fish was collected.

Animals↗

Distinct roles of oncostatin M and leukemia inhibitory factor in the development of primordial germ cells and sertoli cells in mice.

Leukemia inhibitory factor (LIF) stimulates the growth of primordial germ cells (PGCs) in mouse embryo. However, as neither mice lacking LIF nor mice lacking the LIF receptor show defects in PGC growth, an alternate cytokine for PGC growth has been postulated. We investigated the role of mouse oncostatin M (mOSM), which is structurally and functionally related to LIF, in germ cell development. While LIF enhanced the survival of migratory as well as postmigratory PGCs, mOSM acted only on the postmigratory PGCs. Consistent with its biological activity, mOSM was found to be expressed in developing gonads. In the male, Sertoli cells in neonatal testis express mOSM; however, its expression is downregulated in adult testes. Moreover, mOSM enhanced the proliferation of Sertoli cells derived from neonatal testes in vitro more than human OSM or LIF. In contrast, postnatal ovaries do not express mOSM. These results indicate that mOSM is a stage- and sex-specific autocrine growth factor for Sertoli cells.

Animals↗

Changes in gonadal weights, serum lipids, and glucose during maturation in the juvenile northern bobwhite quail (Colinus virginianus).

Changes in serum lipids, serum glucose, and gonadal development during maturation of Colinus virginianus were determined in two trials. In Trial 1, sex, BW, and serum concentrations of total cholesterol, high, low, and very low density lipoprotein cholesterol, triglycerides, and glucose were determined every 2 d from 2 to 14 d and weekly from 21 to 49 d. Relative ovary or testis weights between 14 and 49 d were determined weekly. Body weight increased and all measured serum constituents changed in males and females between 2 and 49 d; however, relative testis weight decreased between 14 and 49 d. In Trial 2, sex, BW, cholesterol, and relative ovary and testis weights were determined in birds at 56 and 63 d of age. The distinctness of external sexual phenotype and its relationship to BW, cholesterol, and relative gonadal weight were also determined at 56 and 63 d. Body weight increased and serum cholesterol decreased in both sexes between 56 and 63 d, but had no association with the distinctness of external sexual phenotype. It was concluded that the development of external sexual identity in male and female Northern Bobwhite quail prior to sexual maturity was not related to changes in BW, gonad weight, serum lipids, or serum glucose before 63 d of age.

Aging↗

Characterization of gonadal sex cord-stromal tumor cell lines from inhibin-alpha and p53-deficient mice: the role of activin as an autocrine growth factor.

Inhibin-alpha-deficient mutant mice have been generated by a targeted deletion of the inhibin-alpha gene through homologous recombination in murine embryonic stem cells. Essentially all of the homozygous mutants develop gonadal sex cord-stromal tumors. To investigate their endocrine and proliferative characteristics, gonadal tumor cells were maintained in vitro. Cells from inhibin-alpha-deficient mice multiplied poorly; however, cells from mice deficient in both inhibin-alpha and p53 proliferated rapidly and showed higher saturation density and plating efficiency, thus allowing the establishment of clonal tumor cell lines. Although negligible estrogen and testosterone was produced by the clonal cells, high levels of progesterone were secreted. A clonal testis tumor cell line (inhibin-alpha/p53 deficient) showed no response to exogenous FSH, human CG (hCG), or inhibin A but exhibited a 6- to 8-fold increase in progesterone production in response to forskolin treatment. The stimulatory effect of forskolin was, however, partially blocked by activin treatment. Northern blot analysis revealed inhibin beta A and beta B mRNA expression in these cells. Furthermore, Western blot analyses indicated the secretion of the beta A-subunit protein. We further tested the role of activin on tumor cell growth. Treatment with follistatin, an activin-binding protein, inhibited tumor cell replication in a dose-dependent manner. In contrast, treatment with activin A stimulated tumor cell growth by itself and partially blocked follistatin action. Incorporation of thymidine into DNA of these cells was also stimulated by activin. In addition, treatment with antiactivin A serum inhibited tumor cell replication and blocked the stimulatory action of activin on cell growth. The activin action is likely mediated by specific receptors because cross-linking of [125]activin to the 50-55 kilodalton type I and 75-80 kilodalton type II receptors was found using sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis. Northern blot analysis also revealed follistatin mRNA expression in the tumor cells, suggesting these cells are related to granulosa cells. Our findings indicate that activin can act as an autocrine growth factor in stimulating the proliferation of gonadal tumor cell lines derived from inhibin-alpha and p53-deficient mice and inhibits progesterone production. These tumor cell lines are useful for studies on the regulation of gonadal cell proliferation and steroidogenesis as well as the signaling pathway mediating activin action.

Activins↗

A human XY female with a frame shift mutation in the candidate testis-determining gene SRY.

The primary decision about male or female sexual development of the human embryo depends on the presence of the Y chromosome, more specifically on a gene on the Y chromosome encoding a testis-determining factor, TDF. The human sex-determining region has been delimited to a 35-kilobase interval near the Y pseudoautosomal boundary. In this region there is a candidate gene for TDF, termed SRY, which is conserved and specific to the Y chromosome in all mammals tested. The corresponding gene from the mouse Y chromosome is deleted in a line of XY female mutant mice, and is expressed at the expected stage during male gonadal development. We have now identified a mutation in SRY in one out of 12 sex-inversed XY females with gonadal dysgenesis who do not lack large segments of the short arm of the Y chromosome. The four-nucleotide deletion occurs in a sequence of SRY encoding a conserved DNA-binding motif and results in a frame shift presumably leading to a non-functional protein. The mutation occurred de novo, because the father of the sporadic XY female that bears it has the normal sequence at the corresponding position. These results provide strong evidence for SRY being TDF.

Amino Acid Sequence↗

Social regulation of the brain-pituitary-gonadal axis.

Reproduction in vertebrates is regulated by the hypothalamic-pituitary-gonadal axis via neural and hormonal feedback. This axis is also subject to exogenous influences, particularly social signals. In the African cichlid fish Haplochromis burtoni, gonadal development in males is socially regulated. A small fraction of the males, which are brightly colored, maintain territories and aggressively dominate inconspicuously colored nonterritorial males. Here we show through manipulation of the social and endocrine environment that changes in social status and gonadal state are accompanied by soma size changes in a population of gonadotropin-releasing hormone-containing neurons in the ventral forebrain. In territorial males, these cells are significantly larger than in nonterritorial males. When an animal switches from being territorial to nonterritorial through a change in social situation, these cells shrink; in animals that change from nonterritorial to territorial status, the cells enlarge. These gonadotropin-releasing hormone-containing cells project to the pituitary and are ultimately responsible for regulating gonadal growth. This mechanism of socially induced cell size change provides the potential for relatively quick adaptive changes in the neuron-endocrine system without nerve cell addition or death. Since the structure of this regulatory axis is conserved among all vertebrates, other species with socially modulated reproductive physiology may exhibit a similar form of physiological regulation.

Animals↗

Connexin43 is expressed in mouse fetal ovary.

Developmental studies have shown that connexin43 (Cx43) is expressed in the ovary from the first day of life and throughout the rest of postnatal development. In both mouse embryonic ovaries and testes, target-directed deletion of Cx43 gene induces a significant decrease in germinal cells, but the exact mechanism determining this reduction remains unknown. Moreover, recently we found that Cx43 is abundantly expressed in mouse testes from the earliest stages of its fetal development. In the present work we investigate whether Cx43 transcript and protein are expressed in mouse embryonic ovaries. Total RNA was analyzed with specific Cx43 oligonucleotides in RT-PCR studies. A Cx43 PCR product was detected in ovaries at 16.5 and 18.5 days postcoitum (dpc). Bands of 43-45 kDa, characteristic of Cx43, were detected in immunoblots of total homogenates of ovaries at 14.5 and 18.5 dpc. Cell type-specific expression of Cx43 was investigated using double-labeled sections incubated with specific antibodies against Cx43 and the enzyme 3beta-hydroxysteroid dehydrogenase (3betaHSD) or a germ cell nuclear antigen (GCNA1), which are cell markers of steroidogenic and germinal cells, respectively. At 18.5 dpc, Cx43 was found in conglomerates of 3betaHSD-positive cells. Cx43 was also localized at homocellular junctions between parenchyma pregranulosa cells, and at heterocellular junctions between pregranulosa and germinal cells. At these two latter localizations, Cx43 was traced back to 12.5 dpc. In conclusion, this study demonstrates for the first time that from the earliest stages of embryonic ovary development, Cx43 is expressed in principal cell types involved in control of female fertility. These data suggest that the gap junctions formed with Cx43 between somatic and germinal cells may be necessary for prenatal expansion of germinal cells at initial stages of fetal gonadal development.

3-Hydroxysteroid Dehydrogenases↗

Differential regulation of luteinizing hormone and follicle-stimulating hormone expression during ovarian development and under sexual steroid feedback in the European eel.

Pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are, in teleosts as in mammals, under the control of hypothalamic factors and steroid feedbacks. In teleosts, feedback regulations largely vary depending on species and physiological stage. In the present study the regulation of FSH and LH expression was investigated in the European eel, a fish of biological and phylogenetical interest as a representative of an early group of teleosts. The eel FSHbeta subunit was cloned, sequenced and together with earlier isolated eel LHbeta and glycoprotein hormone alpha (GPalpha) subunits used to study the differential regulation of LH and FSH. In situ hybridization indicated that FSHbeta and LHbeta are expressed by separate cells of the proximal pars distalis of the adenohypophysis, differently from the situation in mammals. The profiles of LHbeta and FSHbeta subunit expression were compared during experimental ovarian maturation, using dot-blot assays. Expression levels for LHbeta and GPalpha increased throughout ovarian development with a positive correlation between these two subunits. Conversely, FSHbeta mRNA levels decreased. To understand the role of sex steroids in these opposite variations, immature eels were treated with estradiol (E2)and testosterone (T), both steroids being produced in eel ovaries during gonadal development. E2 treatment induced increases in both LHbeta and GPalpha mRNA levels, without any significant effect on FSHbeta. In contrast, T treatment induced a decrease in FSHbeta mRNA levels, without any significant effect on the other subunits. These data demonstrate that steroids exert a differential feedback on eel gonadotropin expression, with an E2-specific positive feedback on LH and a T-specific negative feedback on FSH, leading to an opposite regulation of LH and FSH during ovarian development.

Analysis of Variance↗

Genes involved in testicular development and function.

The development of the testis requires the highly regulated expression of a series of genes. Many of the genes involved are transcription factors, such as steroid hormone receptors and growth factors. Investigators have used gene cloning, mutation analysis, transgenic mice, and gene-deletion studies to define the role of specific genes in testicular development and function. In the past 5 years, investigators have defined a gene on the Y chromosome, SRY, thought to be required for testis determination. This protein is a member of a larger family of related transcription factors. Expression of this gene triggers a cascade of events that leads to the development of the Sertoli cell, Leydig cells, and the testis. The development of the male phenotype is dependent on the presence and action of androgens, which exert their effect after combining with a receptor in the nucleus of the target cell that stimulates gene transcription. Defects in the androgen receptor gene lead to a full spectrum of morphological defects in the male. Interestingly, mutations in other members of the steroid receptor superfamily, such as the estrogen receptor gene, also affect male fertility. A number of "orphan" receptors (i.e., receptors whose ligans have not been identified) are also required for normal testicular development and function, as are several genes normally thought to be tumor-suppressor genes (e.g., Wilms' tumor-suppressor gene). In contrast, alpha-inhibin has been thought to be an endocrine hormone, yet it functions as a tumor-suppressor gene in the testis. Testicular development and normal spermatogenesis require the proper function and coordination of a large number of transcription factors, steroid hormone and orphan receptors, and growth factors. There are likely to be a large number of other, as yet unidentified genes that are necessary for male gonadal development.

Animals↗

European hamsters (Cricetus cricetus) show a transient phase of insensitivity to long photoperiods after gonadal regression.

Annual rhythms of body weight and reproduction in the European hamster (Cricetus cricetus) are the result of an interaction between seasonal changes in day length (photoperiod) and seasonal changes in the responsiveness of animals to these photoperiods. The present study demonstrates that under natural conditions European hamsters are not able to perceive long photoperiods (i.e., a 16L:8D cycle) before mid-November. This is an important difference to other hamster species, in which regrowth of the gonads can be stimulated by exposure to long photoperiods at any stage of gonadal regression. The experiments also demonstrate the existence of an annual phase of sensitivity to long photoperiods that starts around mid-November and extends until March/April. During this phase of sensitivity, exposure to a long photoperiod (16L:8D) induced gonadal regrowth within 3 wk. Additional experiments with an accelerated photoperiodic lighting regimen indicated that a photoperiod of approximately 13 h is necessary to stimulate gonadal regrowth. Under natural light conditions in Stuttgart (48.46 degrees N), a photoperiod of 13 h is reached by the beginning of April, which fits well with the finding that the majority of animals kept under a natural light:dark cycle had well-developed gonads by the end of April. Nevertheless, these animals showed a rather variable timing of gonadal regrowth, ranging from early January to late April. This is most likely the result of two processes: first, an endogenous mechanism (photorefractoriness) that induces gonadal recrudescence without any photoperiodic information while the animals are still in their hibernation burrows, and second, a direct stimulatory effect of long photoperiods.

Animals↗

Expression of the mouse anti-müllerian hormone gene suggests a role in both male and female sexual differentiation.

We describe here the isolation of cDNA and genomic clones corresponding to the mouse gene encoding anti-Müllerian hormone, and the use of these clones as molecular probes to study AMH gene expression. We constructed a 14.5 days post coitum (dpc) mouse fetal testes library and isolated a cDNA clone using bovine, human and rat partial cDNAs as probes. This clone contained a 1 kb insert, which was confirmed by sequencing to be the mouse homologue of AMH. Probes derived from the mouse cDNA clone were used to screen genomic libraries and a 12 kb DNA fragment containing the complete coding region of mouse AMH was isolated. In situ hybridisation was used to determine the precise timing and localisation of AMH expression in male and female embryos and postnatal testes and ovaries. AMH transcripts were first detected in fetal testes at 12.5 dpc when differences between testes and ovaries first become visible. The signal was specific for the Sertoli cells of the testes. Other fetal tissues or female embryos were negative for AMH transcripts. During male development, AMH expression is shut off postnatally. In the female, the expression of AMH was first detected at day 6 after birth and is restricted to granulosa cells. We have correlated the pattern of AMH expression in both sexes with cellular events occurring in gonadal development and discuss some implications that this may have for its function and regulation.

Amino Acid Sequence↗

Disturbance of plasma melatonin profile by high dose melatonin administration inhibits testicular maturation of precocious male masu salmon.

We have previously shown that the testicular development of underyearling male masu salmon Oncorhynchus masou reared under a long photoperiod was accelerated by oral melatonin treatment (0.5 mg melatonin/kg body weight/day), suggesting that melatonin mediates photoperiodic signaling. In this study, we further examined the effects of a disturbance in the plasma melatonin profile on gonadal development in underyearling male masu salmon by administering a higher dose of melatonin. Fish randomly selected in June were divided into two groups. They were reared under a light:dark (LD) cycle of 16:8 (lights on 04:00-20:00 hr) and fed with pellets sprayed with melatonin or vehicle twice a day at 08:30 and at 15:30 hr (7.5 mg melatonin/kg body weight/day) until October. Fish were sampled on Day 0, 25, 60, 90 and 120. The plasma melatonin levels were high in the dark phase and low in the light phase in the control group, while they were constantly high with no significant change in the melatonin-treated group. Melatonin treatment had inhibitory effects on the gonadosomatic index and plasma testosterone levels. Pituitary salmon gonadotropin-releasing hormone content and luteinizing hormone content were significantly lower in the melatonin-treated group on Day 60 and 90, respectively. These results indicate that the plasma melatonin profile is important for mediating photoperiodic signals that regulate brain-pituitary-gonadal axis in underyearling precocious male masu salmon.

Analysis of Variance↗

Gonadal agenesis in XX and XY sisters: evidence for the involvement of an autosomal gene.

Two agonadic sisters, one with a 46,XY and the other with a 46,XX karyotype, both with normal female external genitalia and hypoplastic Müllerian derivatives, born to a consanguineous marriage, were studied from a clinical, endocrinological, histological, and genetic perspective. Using PCR amplification, Southern hybridization, and DGGE analysis, it was found that the XY patient had no mutations in the conserved sequence of the SRY gene, the putative testis-determining gene in mammals, whereas her XX affected sister is SRY-negative. To our knowledge, this is the first report of XY and XX sibs in familial gonadal agenesis without other somatic abnormalities. The involvement of an autosomal locus impeding gonadal development in both sexes is discussed.

Adult↗

Biochemical and histological responses in mussel (Mytilus edulis) exposed to North Sea oil and to a mixture of North Sea oil and alkylphenols.

Several environmental chemicals are suspected to be responsible for adverse health effects on the reproductive system in various organisms. During this work, environmentally relevant concentrations of North Sea oil were used alone or in combination with alkylphenols and additional PAH to study the effect on vitellogenin-like protein expression and gonadal development in mussels. North Sea oil (0.5 ppm) induced the expression of phospho-proteins in both sexes indicating that some compounds are oestrogen-mimics. This induction was not seen in samples dosed with the mixture but signs of toxic effects were observed in the gonads. Indeed, numerous degenerating ovarian follicles in females and foci, similar to vertebrate melanomacrophage centres, were observed in testes.

Animals↗

Maternal diet influences reproductive development in male prairie vole offspring.

The plant compound, 6-methoxy-2-benzoxazolinone (6-MBOA), is found in the meristematic tissue of young, vegetatively growing grasses, and its ingestion stimulates the reproductive system of rodents in both short and long photoperiods. The present study demonstrates the existence of a novel mechanism whereby the presence of 6-MBOA in the diet of pregnant prairie voles (Microtus ochrogaster) enhances gonadal development in their male offspring. Female voles were fed specially milled food in which 6-MBOA was present (50 micrograms of 6-MBOA/g food) or absent (0 microgram of 6-MBOA/g food) prior to the birth of their young; all of these dams received a diet that lacked 6-MBOA/g after the pups were born. Other females were fed food without 6-MBOA throughout pregnancy, but received one of the two diets during lactation. The pups from all experimental groups were weaned at 3 weeks of age and fed thereafter one of the two diets for 3 additional weeks. Prenatal exposure to 6-MBOA enhanced male reproductive development. Maternal ingestion of 6-MBOA during lactation or postweaning intake of 6-MBOA by the young did not influence reproductive development of males. This mechanism may be involved in the rapid rate of sexual maturation observed prior to peak population densities of microtine rodents.

Animals↗

Ontogeny of gonadotropin receptors in the fetal and neonatal rat testis.

To evaluate the extent to which LH receptors may participate in the regulation of testosterone production by the fetal and neonatal rat testis, the gonadal content of LH receptors was determined and correlated with the gonadal content of testosterone and other steroids at daily intervals throughout the period of sexual differentiation and early neonatal life. Also, to determine if FSH has a potential role during fetal life, FSH receptors were measured from 14.5 until 21.5 days of gestation, just before birth. LH receptors were first detected in the fetal rat testis at 15.5 days of gestation, at a concentration of 0.072 +/- 0.016 fmol/gonad. This is the time at which previous studies have shown a biological response to LH stimulation with increases in cAMP and testosterone production. LH receptor content remained constant from 15.5-17.5 days of gestation and then increased sharply at 18.5 days of gestation to 0.706 +/- 0.046 fmol/gonad, coincident with a surge in the testosterone content of the fetal testis. LH receptor content continued to rise until birth, reaching a maximum level of 2.00 +/- 0.24 fmol/gonad at 21.5 days of gestation, and did not significantly differ from this value through 5 days after birth, whereas intratesticular testosterone content decreased after birth. FSH receptors could be measured from 17.5 days of gestation, but remained very low through 19.5 days of fetal life. At 20.5 days, FSH receptor levels began to rise sharply and continued to increase through 21.5 days of gestation, just before birth. These data show that LH receptors are measurable at the time when the fetal testis becomes responsive to LH stimulation. It is possible that the increase in LH receptors may act as a mechanism for amplification of the stimulatory effect of low circulating LH levels on the fetal testis being concomitant with the intratesticular testosterone increase at the same stage. The decrease in testosterone production after birth cannot be attributed to a decrease in LH receptors in the neonatal gonad. Since 5 alpha-reduced androgens increase after birth, other possibilities, such as alternative steroid pathways, are a more likely explanation for the decrease in testosterone content. The presence of FSH receptors in the fetal testis imply that this hormone may have a function in the developing gonad, particularly in the last 2 days of fetal life.

Aging↗