Influence Of Follicle-stimulating Hormone Research Articles

Effects of follicle-stimulating hormone on the proliferation and apoptosis of infantile hemangioma stem cells

ObjectiveTo investigate the effects of different concentrations of follicle-stimulating hormone (FSH) on the proliferation and apoptosis of human hemangioma stem cells, it will provide a basis for studying the mechanism of FSH in treating hemangioma. MethodsHemangioma specimens were collected from the Longgang District Maternity & Child Healthcare Hospital of Shenzhen City. Hemangioma stem cells were treated with different concentrations of FSH. Cell viability was detected by CCK8 method and cell apoptosis was analyzed by flow cytometry. ResultsHemangioma stem cells (HemSCs) were extracted from fresh tissue of infantile hemangioma by the CD133 immunomagnetic bead method. Under the influence of FSH at different concentrations (0, 100, 1000 IU/L), the cell viability of hemangioma stem cells increased significantly in a concentration-dependent manner (P < 0.05). At the same time, the apoptosis of hemangioma stem cells decreased with increasing concentrations of follicle-stimulating hormone (P < 0.05). Specifically, 1000 IU/L FSH significantly promoted the proliferation of hemangioma stem cells and inhibited their apoptosis. ConclusionHigh concentration of follicle-stimulating hormone can maintain the growth of hemangioma by promoting the proliferation and inhibiting the apoptosis of hemangioma stem cells.

Sphingosine-1-phosphate regulation of luteinising hormone-induced steroidogenesis and proliferation of bovine theca cells in vitro.

Sphingosine-1-phosphate (S1P) is synthesised by follicle granulosa cells under the influence of follicle-stimulating hormone and seems to be necessary for the biological effects of this gonadotrophin. To determine if luteinising hormone (LH) increases S1P production and if this sphingolipid, either induced by LH or added to culture media, regulates steroidogenesis and cell viability in bovine theca cells. We used bovine theca cell cultures treated with: S1P (0, 0.1, 1 and 10μM; Experiment 1), LH (0, 0.02, 0.2 and 2ngmL-1; Experiment 2) and LH (0.02ngmL-1) plus a sphingosine kinase inhibitor (SKI-178; 0, 5 and 10μM; Experiment 3). Treatment with S1P did not affect (P>0.05) theca cell viability or their ability to produce progesterone and testosterone. LH (0.02ngmL-1) increased (P<0.05) S1P production, and stimulated the expression of phosphorylated sphingosine kinase-1 (pSPHK1). However, the inhibition of SPHK1, by a specific SPHK1 inhibitor (SKI-178), reduced (P<0.05) cell viability and progesterone secretion. Additionally, the use of SKI-178 increased theca cell testosterone production (P<0.05). S1P added to culture media did not affect cell viability or steroid synthesis. However, LH stimulated the production of S1P, by increasing phosphorylation of SPHK1 in theca cells. This intracellular S1P was inhibitory on testosterone production but augmented progesterone and viable cell number. These results suggest a novel signalling pathway for LH in theca cells and underline the importance of S1P in the regulation of steroid synthesis.

Actions and Roles of FSH in Germinative Cells.

Follicle stimulating hormone (FSH) is produced by the pituitary gland in a coordinated hypothalamic–pituitary–gonadal (HPG) axis event, plays important roles in reproduction and germ cell development during different phases of reproductive development (fetal, neonatal, puberty, and adult life), and is consequently essential for fertility. FSH is a heterodimeric glycoprotein hormone of two dissociable subunits, α and β. The FSH β-subunit (FSHβ) function starts upon coupling to its specific receptor: follicle-stimulating hormone receptor (FSHR). FSHRs are localized mainly on the surface of target cells on the testis and ovary (granulosa and Sertoli cells) and have recently been found in testicular stem cells and extra-gonadal tissue. Several reproduction disorders are associated with absent or low FSH secretion, with mutation of the FSH β-subunit or the FSH receptor, and/or its signaling pathways. However, the influence of FSH on germ cells is still poorly understood; some studies have suggested that this hormone also plays a determinant role in the self-renewal of germinative cells and acts to increase undifferentiated spermatogonia proliferation. In addition, in vitro, together with other factors, it assists the process of differentiation of primordial germ cells (PGCLCs) into gametes (oocyte-like and SSCLCs). In this review, we describe relevant research on the influence of FSH on spermatogenesis and folliculogenesis, mainly in the germ cell of humans and other species. The possible roles of FSH in germ cell generation in vitro are also presented.

Follicle stimulating hormone and estradiol alter immune response in osteoarthritic mice in an opposite manner.

Although a number of studies have shown that the occurrence and progression of osteoarthritis (OA) is related to endocrine system dysfunction, there is limited evidence about what roles sex hormones play. The aim of the present study was to examine the capacity of 17β-estradiol (ED) and follicle stimulating hormone (FSH) to alter the differentiation of bone marrow (BM) cells in arthritic mice. The experiments were conducted in collagenase-induced osteoarthritis in mice. Cartilage degradation was observed by safranin and toluidine blue staining. Flow cytometry was used to define different BM and synovial cell populations. The influence of FSH and ED on osteoclastogenesis was studied in BM cultures and on the osteoblastogenesis in primary calvarial cultures. The levels of IL-8, TNF-α, FSH, and osteocalcin were estimated by ELISA. FSH increased cartilage degradation and serum osteocalcin levels, while ED abolished it and lowered serum osteocalcin. FSH elevated the percentage of monocytoid CD14+/RANK+ and B cell CD19+/RANK+ cells in contrast to ED which inhibited the accumulation of these osteogenic populations. Also, ED changed the percentage of CD105+/F4/80+ and CD11c+ cells in the synovium. FSH augmented and ED suppressed macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast (OC) formation, and this correlated with a respective increase and decrease of IL-8 secretion. FSH did not influence osteoblast (OB) formation while ED enhanced this process in association with changes of TNF-α, IL-8, and osteocalcin production. ED reduced osteoclast generation in bone. The key outcome of the current study is that both hormones influenced BM cell differentiation, with FSH favoring osteoclast formation and ED favoring osteoblast accumulation.

Nuclear receptors: Key regulators of somatic cell functions in the ovulatory process

The development of the ovarian follicle to its culmination by ovulation is an essential element of fertility. The final stages of ovarian follicular growth are characterized by granulosa cell proliferation and differentiation, and steroid synthesis under the influence of follicle-stimulating hormone (FSH). The result is a population of granulosa cells poised to respond to the ovulatory surge of luteinizing hormone (LH). Members of the nuclear receptor superfamily of transcription factors play indispensable roles in the regulation of these events. The key regulators of the final stages of follicular growth that precede ovulation from this family include the estrogen receptor beta (ESR2) and the androgen receptor (AR), with additional roles for others, including steroidogenic factor-1 (SF-1) and liver receptor homolog-1 (LRH-1). Following the LH surge, the mural and cumulus granulosa cells undergo rapid changes that result in expansion of the cumulus layer, and a shift in ovarian steroid hormone biosynthesis from estradiol to progesterone production. The nuclear receptor best associated with these events is LRH-1. Inadequate cumulus expansion is also observed in the absence of AR and ESR2, but not the progesterone receptor (PGR). The terminal stages of ovulation are regulated by PGR, which increases the abundance of the proteases that are directly responsible for rupture. It further regulates the prostaglandins and cytokines associated with the inflammatory-like characteristics of ovulation. LRH-1 regulates PGR, and is also a key regulator of steroidogenesis, cellular proliferation, and cellular migration, and cytoskeletal remodeling. In summary, nuclear receptors are among the panoply of transcriptional regulators with roles in ovulation, and several are necessary for normal ovarian function.

Clinical effect of three doses of mifepristone on patients with dysfunctional uterine bleeding

Objective To explore the clinical effect of three doses of mifepristone on patients with dysfunctional uterine bleeding. Methods 150 patients with dysfunctional uterine bleeding were chosen, and they were randomly divided into 3 groups, including low dose group (50 patients), middle dose group (50 patients) and high dose group (50 patients). All patients adopted routine treatment.On the basis of this, the low dose group received 6.25mg/d mifepristone, the middle dose group received 12.5mg/d mifepristone, the high dose group received 18.25mg/d mifepristone, continued 6 months.The influence of follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E), progesterone (P), volume of uterine and endometrail thickness of patients were observed. Results After treatment, the FSH, LH, E and P levels in the three groups were significantly decreased compared with before treatment (FSH: t=4.406, 5.329, 3.610, LH: t=4.563, 6.134, 4.455, P=0.000, 0.000, 0.000; P=0.000, 0.000, 0.000; E: t=7.173, 6.815, 7.018, P=0.000, 0.000, 0.000; E: t=2.367, 6.315, 4.351, P=0.020, 0.000, 0.000), and the difference were statistically significant (all P 0.05). Compared with the low dose group, E levels in the middle dose group and high dose group significantly decreased(t=3.850, 2.085, P=0.000, 0.004). Before and after treatment, the uterine volume among the three groups had no significant difference (P>0.05). After treatment, the functional uterine bleeding symptoms were significantly relieved in the three groups, the effective rate was 100%.The recurrence rate of the low dose group was 32%, which was significantly higher than 8% and 10% of the middle dose group and high dose group.The amenorrhea rate of the middle dose group and high dose group(6% and 2%) was significantly lower than that of the low dose group (46%). Conclusion The treatment of 12.5mg/d mifepristone is effectively adapted to patients with dysfunctional uterine bleeding. Key words: Mifepristone; Uterine bleeding; Dose-respone relationship, drug

Primordial Follicles Development of Immature Mice Ovary after FSH and Ovary Cutting Treatments

The aims of the study were to investigate the influence of FSH and the ovary cutting treatments on the development of primordial follicles into preantral and antral follicles. Ovaries were grouped as whole ovary (without cutting); partially cut ovary and completely cut ovary (hemi ovary). All ovary groups were cultured in Dubellco’s Modified Eagle Medium (DMEM) containing 5ug/ml insulin, 10ug/ml transferrin, 5ug/ml selenium (ITS), 5% FBS, 50ug/ml gentamycin with and without 100uIU/ml Follicle Stimulating Hormone (FSH). Cultures were done in 5% CO2 incubator at 37oC. Results showed that after 8 days in vitro cultured in DMEM containing FSH, the average number of preantral follicles isolated from each whole, partially-cut and completely-cut ovaries were 16.1 + 3.3, 26.8 ± 7.7 and 12.3 + 1.9, respectively. On the other hand, those cultured in DMEM without FSH they were 17.3 + 3.8, 23.3 ± 5.2 and 17.8 + 2.8, respectively. After additional cultured for 8 days, the percentage of preantral follicles developing into the antral follicles in DMEM with and without FSH were 26.7 + 5.7 and 11.7 + 2.9, respectively. In conclusion, the supplementation of FSH in the culture medium did not increase the number of preantral follicles, but significantly increased the number of antral follicles. The ovary cutting treatment significantly increased the average number of collected preantral follicles.

Developmentally distinct in vivo effects of FSH on proliferation and apoptosis during testis maturation

The critical influence of follicle stimulating hormone (FSH) on male fertility relates both to its impact on Sertoli cell proliferation in perinatal life and to its influence on the synthesis of Sertoli cell-derived products essential for germ cell survival and function in the developing adult testis. The nature and timing of this shift of germ cells to their reliance on specific Sertoli cell-derived products are not defined. Based on existing data, it is apparent that the dominant function of FSH shifts between 9 and 18 day postpartum (dpp) during the first wave of spermatogenesis from driving Sertoli cell proliferation to support germ cells. To enable comprehensive analysis of the impact of acute in vivo FSH suppression on Sertoli and germ cell development, FSH was selectively suppressed in Sprague-Dawley rats by passive immunisation for 2 days and/or 4 days prior to testis collection at 3, 9 and 18 dpp. The 3 dpp samples displayed no measurable changes, while 4 days of FSH suppression decreased Sertoli cell proliferation and numbers in 9 dpp, but not 18 dpp, animals. In contrast, germ cell numbers were unaffected at 9 dpp but decreased at 18 dpp following FSH suppression, with a corresponding increase in germ cell apoptosis measured at 18 dpp. Sixty transcripts were measured as changed at 18 dpp in response to 4 days of FSH suppression, as assessed using Affymetrix microarrays. Some of these are known as Sertoli cell-derived FSH-responsive genes (e.g. StAR, cathepsin L, insulin-like growth factor binding protein-3), while others encode proteins involved in cell cycle and survival regulation (e.g. cyclin D1, scavenger receptor class B 1). These data demonstrate that FSH differentially affects Sertoli and germ cells in an age-dependent manner in vivo, promoting Sertoli cell mitosis at day 9, and supporting germ cell viability at day 18. This model has enabled identification of candidate genes that contribute to the FSH-mediated pathway by which Sertoli cells support germ cells.

Follicle stimulating hormone-induced growth promotion and gene expression profiles on ovarian surface epithelial cells.

Epidemiologic data have implicated reproductive follicle-stimulating hormone (FSH) as a probable risk factor for ovarian cancer (OC) development. Although pituitary and sex hormones have been reported to regulate OC cell growth, no information is available on the influence of FSH on gene expression profiles during ovarian surface epithelial (OSE) cell proliferation. This study evaluated the effect of FSH treatment on cell proliferation of various OSE cell lines and gene expression profiles with FSH treatment. Follicle-stimulating hormone receptor (FSHR) was found at higher expression at both transcriptional and protein levels in ovarian cancerous tissues compared to normal tissues, and FSH was shown to promote cell growth in 3 OSE cell lines. Furthermore, it was also found that overexpression of FSHR in Chinese hamster ovary (CHO) cells leads to cell proliferation. Using cDNA MicroArray analysis on MCV152 cells with FSH treatment, 91 genes were found upregulated and 68 genes downregulated for more than 2-fold after FSH treatment. Most of the genes were related to metabolism, cell proliferation and oncogenes. Downregulated genes included tumor suppressor genes (RB1, BRCA1, BS69) and the genes related to cell proliferation control. Pathway analysis found that FSH activates certain important enzymes in sterol biosynthesis pathways. FSH-induced gene expression profiles on MCV152 cells support the standing hypothesis that FSH is a probable risk factor for ovarian cancerous development.

Spermiogenesis in commercial poultry species: anatomy and control

Spermatogenesis is a complicated process dependent upon several factors. Formation of a testis requires the interaction of gene-products and hormones (androgens) on pluripotent tissue. In birds, the female is the heterogametic (ZW) sex, but W chromosomal genes do not influence gonadal development in a way similar to the SRY gene on the mammalian Y chromosome. However, autosomal genes such as SRY-like HMG box gene 9 (SOX9) may influence gonadal development. Hormones affect development; male gonads subjected to estrogen form an ovotestis, whereas ovaries exposed to aromatase inhibitors form an atypical testis. Sertoli cell numbers are set early in spermiogenesis, possibly under the influence of follicle-stimulating hormone and thyroid hormone, and this may determine the number of gonial cells that can be supported. Sertoli cells make a number of substances that affect testicular development and function, particularly anti-Mullerian hormone, which inhibits female oviduct formation from the Mullerian anlage, inhibits aromatase activity to stop estrogen production, and possibly stimulates androgen production by Leydig cells. Undifferentiated primordial germ cells (PGC) migrate to the testis and are converted to spermatogonia by factors from gonadal ridge tissue and androgens. The PGC of males in the ovary form oocytes of Z genotype, whereas the female PGC in males form mostly Z sperm (with a few of W genotype). Transmission electron microscopy micrographs of turkey testis are presented, and control of spermatogenesis by hormones and cytokines is discussed. This discussion includes follicle-stimulating hormone, luteinizing hormone, inhibin, activin, follistatin, tumor necrosis factor-alpha, growth factors such as transforming growth factor-beta, interleukins, and interferon. Although information concerning paracrine and autocrine regulation of the avian testis by these substances is sparse, much can be learned from mammalian studies, in which putative roles of each of these substances have been established. How Sertoli cells cause directed apoptosis of spermatogonia using the Fas-ligand, Fas-receptor pathway is reviewed, as well as ways to circumvent this process. A possible role for ubiquitin concerning prevention of heat-induced damage to the testis is presented.

The role of estradiol in primate ovarian function

Two-cell, two-gonadotrophin interactions within the ovarian follicle involve stimulating theca cells with luteinizing hormone (LH) to produce androgens which enter granulosa cells where, under the influence of follicle stimulating hormone (FSH), they are aromatized to estradiol. In nonprimate species, autocrine and paracrine functions for estradiol within the follicle have been shown to mediate the trophic effects of FSH on granulosa cells resulting in proliferation, increased expression of FSH receptors, antrum formation, induction of LH receptors, and inhibition of apoptosis. The axiom that estradiol is particularly necessary for follicular growth and maturation has been routinely adopted and perpetuated for decades in discussions on the regulation of follicular function in primates. Focus on the level of estradiol in follicular fluid as an index of follicle, and hence oocyte, quality by many investigators yielded conflicting results. Nonetheless, development of ovarian stimulation protocols that employ exogenous administration of both FSH and LH for the treatment of infertility in women rely on the correlation between the growth of multiple follicles and increasing serum levels of estradiol to predict a successful outcome. Initial reports of rare conditions causing defects in follicular estradiol biosynthesis, such as with P450-17αhydroxylase/17,20 lyase deficiency, associated the disruption of follicular development with estradiol deprivation. However, the elevated levels of gonadotrophins also observed in these patients rather than the absence of intrafollicular estradiol may have led to the dysregulation of folliculogenesis. Evidence to counter the notion that follicles can only grow in an estradiol-replete environment was provided by studies of women with hypogonadal hypogonadism and of medically hypophysectomized macaques, wherein low levels of estradiol were accompanied by induction of multiple preovulatory follicles upon treatment with urinary preparations of FSH alone. Unfortunately, there are no data available from these studies on oocyte performance under conditions of low estradiol resulting from steroidogenic enzyme deficiencies or hypogonadal hypogonadism. Recent studies of steroid-depleted as well as hypogonadal women and macaques reinvestigated the hypothesis that estradiol plays a pivotal role in folliculo- and gametogenesis in primates and are discussed below.

Naturally Occurring Mutations of the Luteinizing-Hormone Receptor: Lessons Learned about Reproductive Physiology and G Protein–Coupled Receptors

The luteinizing hormone (LH) receptor (LHR) is a heptahelical receptor present primarily in the ovaries of females and the testes of males. This same receptor can bind with high affinity either pituitary LH or the nearly identical placental hormone human chorionic gonadotropin (hCG). In both males and females, the levels of LH remain quite low during childhood years, until puberty, at which time the hypothalamic-pituitary-gonadal axis matures. After puberty, the functions of LH are critical to normal reproductive function. In postpubertal males, LH stimulates testosterone synthesis in the Leydig cells of the testes, which, in turn, is necessary for both formation of male secondary sexual characteristics and spermatogenesis. In nonpregnant postpubertal females, LH plays several roles. During the follicular phase of the ovarian cycle, LH stimulates theca cells to synthesize androgens, which are then aromatized into estradiol in granulosa cells under the influence of follicle-stimulating hormone (FSH). The midcycle surge of LH induces follicular maturation and ovulation. Subsequently, during the luteal phase, LH induces the formation of the corpus luteum and stimulates progesterone synthesis. In the pregnant female, placental hCG binds to the LHR on ovarian luteal cells and causes the corpus luteum, which otherwise undergoes atresia, to be maintained and to continue steroid synthesis, which is necessary for the continuation of pregnancy. During pregnancy, if the fetus is male, placental hCG also stimulates fetal testicular Leydig cells to produce testosterone, which, in turn, mediates the differentiation of the external genitalia and induces the descent of the testes (see Roberts et al. 1999 [in this issue]). Clearly, the LHR plays a critical role in reproductive physiology in both males and females. The importance of the LHR signal-transduction pathway in normal reproductive functioning has been further underscored by the discovery, in recent years, of naturally occurring mutations of the human LHR gene, hLHR.

FSH inhibits the augmentation by oestradiol of the pituitary responsiveness to GnRH in the female rat.

The effect of follicle stimulating hormone (FSH) treatment on the pituitary response to gonadotrophin-releasing hormone (GnRH) was studied in rats in various reproductive conditions. A 3-day treatment of cycling rats with FSH (Metrodin; 10 IU/injection) lowered the spontaneous pre-ovulatory. LH-surge and suppressed the pituitary luteinizing hormone (LH) response to GnRH. FSH also suppressed the LH response of pseudopregnant (PSP) rats on day 8 of pseudopregnancy, but not that of day-8 PSP rats which had been ovariectomized on day 4 (OVX-PSP rats). GnRH induced self priming in cycling, PSP and OVX-PSP rats. Oestradiol strongly augmented the pituitary LH-response to GnRH injection in PSP and OVX-PSP rats, but not in cycling rats; probably because in these latter animals the LH response to GnRH was already augmented by endogenous oestradiol. FSH suppressed the LH response to GnRH in oestradiol-treated PSP and cycling rats; in these latter rats the suppression of the LH response was as strong as that in cycling rats not treated with oestradiol. FSH did not suppress the LH response of oestradiol-treated OVX-PSP rats. The effect of FSH was not associated with changes in plasma oestradiol and progesterone concentrations. Analysis of the data revealed that FSH specifically suppressed the augmentative effect of oestradiol, but did not affect the GnRH-self priming effect. It is concluded that under the influence of FSH, the ovaries produce a factor which suppresses the augmentative effect of oestradiol on the GnRH-induced LH response of the pituitary gland. It is suggested that this effect of FSH underlies the suppression of the spontaneous LH-surges of FSH-treated cycling rats. As the present putative 'oestrogen-antagonizing factor' did not suppress the GnRH-self priming effect, it is suggested that this factor is not identical to gonadotrophin surge inhibiting factor.

Effect of bovine follicular fluid administration during or after norgestomet treatment on the fate of the proestrus dominant follicle in heifers

Abstract The objective was to examine the influence of follicle stimulating hormone (FSH) on the maintenance and ovulation of the proestrus dominant follicle (DF) in cattle. This was investigated by subjecting a proestrus DF, maintained by a single norgestomet (N) implant, to bovine follicular fluid (BFF) injections during N treatment and immediately after its removal. Earlier, we demonstrated that with an insertion of a single N implant the proestrus DF could be maintained for 9 days without affecting its ovulatory capacity. Eighteen cycling Holstein heifers were treated with a N implant at proestrus. The day of implant insertion was designated day 1 of the implant period and the implant was retained for 9 days. Heifers ( n = 6 per group) were randomly allocated to receive saline for 4 days from day 5 to day 8 of the implant period and for 4 days from the day of implant removal to day 3 after removal (CONTROL) or BFF from day 5 to day 8 of implant period (BFF-DURING) or BFF from the day of implant removal to day 3 after implant removal (BFF-AFTER). Injections (10 ml) were given i.v. twice daily and the ovaries monitored by ultrasonography daily, throughout and after the implant period. All CONTROL heifers maintained the DF during treatment and ovulated following implant withdrawal. In all BFF-DURING heifers, the BFF injections caused regression of the DF and its disappearance. In three of the BFF-AFTER heifers, BFF injections caused regression of the DF. In the remaining three BFF-AFTER heifers, the DF ovulated. Mean plasma FSH concentrations did not differ ( P > 0.05) between the CONTROL and BFF-DURING heifers. However, the mean plasma FSH concentrations were lower in BFF-AFTER heifers compared with CONTROLS ( P P > 0.05). In summary, BFF treatment caused atresia of the proestrus DF when maintained by N and this was not associated with suppression of circulating FSH. Administration of BFF after implant removal resulted in an equal chance of ovulation or regression of DF. Regression was associated with suppression of FSH and LH.

Influence of follicle stimulating hormone on in vitro maturation and cleavage of buffalo ( [formula omitted]) oocytes after in vitro fertilization

Influence of follicle stimulating hormone on in vitro maturation and cleavage of buffalo ( [formula omitted]) oocytes after in vitro fertilization

Regulation of expression of Xenopus vitellogenin genes.

The assembly of the developing egg is a fascinating example of division of labor among oocytes and other tissues, with the coordination of activities in different tissues being achieved by hormones. Among nonoocyte tissues are (1) the follicle cells, which, under the influence of follicle-stimulating hormone (FSH), synthesize and release the sex steroids estrogen and progesterone; (2) the oviduct, which produces egg white proteins, coat proteins, or egg-sustaining fluids and whose activity is regulated by both steroid hormones; and (3) the liver, which, under the sole control of estrogen, provides the developing egg with yolk proteins, cholesterol, phospholipids, and lipoproteins. The participation of the oviduct and liver is particularly pronounced in nonmammalian species with free-living embryos, as in birds and amphibia.

Influence of follicle-stimulating hormone on glucose transport by cultured Sertoli cells.

Transport of 3-O-methyl-D-[14C]glucose by Sertoli cells cultured in plastic dishes, is competitively inhibited by glucose (Ki 4 microM). The glucose analogue was therefore used to study glucose transport in these cells in which it is not metabolized. Addition of follicle-stimulating hormone (FSH) (10 micrograms/ml) or dibutyryl cyclic AMP (1 mM) to the cells, increases transport of methylglucose by Sertoli cells. The increased transport results from increased influx and involves decrease in Km without change in Vmax. These changes in the kinetics of transport are seen with both FSH and dibutyryl cyclic AMP. FSH does not stimulate transport of methylglucose in peritubular fibroblasts nor in germ cells. In view of the importance of lactate as a substrate for spermatids (Mita and Hall, 1982) it is proposed that stimulation of the transport of glucose by Sertoli cells in response to FSH is important in the increased production of lactate by these cells in response to FSH and hence is one mechanism by which the tropic hormone enables the Sertoli cell to promote spermatogenesis.

Metabolism of testosterone by human granulosa cells in culture: Influence of follicle-stimulating hormone and luteinizing hormone

Human granulosa cells were isolated from follicles (8 to 15 mm) and cultivated for 24 hours in the presence or absence of follicle-stimulating hormone (NIH-FSH-HS-1, 1 microgram/ml) and luteinizing hormone (NIAMDD-hLH-1, 1 microgram/ml). Testosterone -4-14C was added subsequently to all cultures for 4-, 6-, and 24-hour periods. Of the seven metabolites of testosterone studied, 17 beta-estradiol (E2) and estrone (E1) were the major products. In all patients, levels of E2 were three to ten times higher than those of E1. Production of E2, but not E1, was stimulated by either follicle-stimulating hormone (FSH) or luteinizing hormone (LH). The cells of the largest follicle (15 mm) showed greater response to LH than to FSH. Production of the other C19 and C18 metabolites was very low or negligible. These results further suggest that FSH regulates the aromatization of testosterone in human granulosa cells, and that LH may have the same effect on the matured follicle during the preovulatory period.

The influence of follicle-stimulating hormone on testicular phospholipids

The influence of follicle-stimulating hormone on testicular phospholipids

INFLUENCE OF FOLLICLE-STIMULATING HORMONE ON THE ESTIMATION OF LUTEINIZING HORMONE IN THE VENTRAL PROSTATE AND OVARIAN ASCORBIC ACID DEPLETION ASSAYS.

The influence of ovine pituitary follicle-stimulating hormone (FSH) on the measurement of ovine pituitary luteinizing hormone (LH) in the ovarian ascorbic acid depletion (OAAD) and the ventral prostate weight (VPW) assays was examined. It was found that potentiation of ovine luteinizing hormone (NIH-LH-S1) was induced in the OAAD method by ovine follicle-stimulating hormone (NIH-FSH-Sl) when the latter hormone was present in sufficiently high concentration (FSH: LH =30:1 and 100:1). In the VPW assay, the activity of NIH-LH-Sl was not increased by ovine NIH-FSH-Sl at ratios of FSH:LH ranging from 1:1 to 30:1. (Endocrinology 76: 1150, 1965)