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PubMed1994

Expression of FSH in CHO cells, I. Comparison of promoter types and effects of their respective inducers.

The expression levels of recombinant human follicle stimulating hormone (r-hFSH) were studied in several CHO-Kl derived cell lines. The cell lines varied in the promoter used to control r-hFSH expression and in the subunit gene copy ratio. FSH is a heterodimeric molecule, with 2 N-glycosylation sites per peptide chain, and shares a common alpha subunit with the other gonadotropins. Serum stimulated FSH production in the beta actin promoter cell lines 2-3 times over the 7-10 ng/10(6) cells/h levels obtained in protein-free medium. Serum seemed to have roles other than purely at the transcriptional level judging by the increased free alpha to dimer ratio secreted from cells cultured in serum-free medium. Zinc induced FSH expression in metallothionein cell lines, with a 3-fold induction at 50 microM concentrations compared to 0 microM zinc, giving specific productivities of about 7-10 ng/10(6) cells/h, but the induction kinetics were complicated, and suggested other roles for zinc in addition to activation of the metallothionein promoter. Evidence suggested significant post-transcriptional regulation of FSH expression.

Actins↗
PubMed1986

Relationships between serum FSH level and the size of testis in azoospermic patients.

Sixty-eight out of 700 patients proved to be azoospermic at our Andrology Clinic between 1981 and 1983. According to the serum FSH level and testis size, three main diagnostic groups were established: 1. patients with occlusion but testis size and FSH level normal; 2. patients with smaller testis size and increased FSH level and primary spermatogenetic disorder; 3. non-palpable testis and increased serum FSH level referring also to testicular disorder. No correlations were found between serum LH and testosterone levels and testicular volume.

Follicle Stimulating Hormone↗
PubMed1981

The effect of oral estrogen therapy on serum FSH and LH levels in young women with hyper-gonadotrophic ovarian failure.

Fourteen women, 18--46 years old (median age: 28 years) with hypergonadotrophic ovarian failure were each treated daily for 21 days with 10 micrograms, 20 micrograms, 40 micrograms, and 60 micrograms ethinyl estradiol, 2,000 micrograms estriol, and 1,250 micrograms conjugated estrogens in six or more consecutive treatment cycles in a randomly assigned sequences. Before treatment and at the beginning of the 3rd week of each of the mentioned estrogen regimens, basal serum FSH and LH levels were measured. During the last 5 days of each treatment cycle, 10 mg of oral norethisterone acetate were given in addition to the estrogen, and after a treatment-free interval of 7 days the next estrogen regimen was begun according to the random list. FSH values were inversely related to the various dosages of ethinyl estradiol; the upper normal range with the exception of the periovulatory phase was reached with 40--60 micrograms ethinyl estradiol. FSH levels during treatment with 1250 micrograms of conjugated estrogens were similar to those found during treatment with 20 micrograms ethinyl estradiol. When 2,000 micrograms of estriol were given daily, FSH levels rose of pretreatment values. LH behaved similarly except that during treatment with 2,000 micrograms of estriol and 10 micrograms of ethinyl estradiol values above pretreatment levels were found.

Administration, Oral↗
PubMed2006

Mechanism delineating differential effect of an antiestrogen, tamoxifen, on the serum LH and FSH in adult male rats.

Tamoxifen, a synthetic non-steroidal antiestrogen with residual estrogenic activity, administered to adult male rats reduces their fertility. A decrease in the circulating LH and testosterone levels with a transient rise or no change in circulating FSH levels was observed. The present study was carried out to delineate the mechanism causing the differential effect of tamoxifen on circulating gonadotropins by correlating it to changes in the hypothalamic LHRH, pituitary gonadotropins and testicular inhibin/activin. Hypothalamus, pituitary-hypothalamus complex (PHC) and intact pituitary (PI) from control and tamoxifen-treated male rats were superfused in vitro, and pulsatile release of LHRH by hypothalamus and that of LH and FSH by the PHC and PI were studied. Concomitantly, testicular immunoexpression of alpha and betaB subunits of inhibin/activin were studied by immunohistochemistry and enzyme-linked immunosorbent assays (ELISA). At 0.4 mg/kg/day dose of tamoxifen a decrease in mean hypothalamic LHRH and LH pulse frequency from PHC construct was observed. FSH pulse frequency was not affected under the same experimental conditions. At the same dose of tamoxifen, testicular expression of both alpha and betaB subunits of inhibin/activin was upregulated. The study demonstrated that reduced circulating LH levels were due to a decrease in hypothalamic LHRH concentration and in LH pulsatility following tamoxifen treatment. The lack of effect on circulating FSH under the same experimental conditions was likely due to its modulation by inhibin and activin.

Activins↗
PubMed2005

Differences in serum LH and FSH levels using depot or daily GnRH agonists in controlled ovarian stimulation: influence on ovarian response and outcome of ART.

PURPOSE: To study effects of endogenous LH levels on ovarian response and outcome in ART cycles a controlled study was performed with two patient groups differing in the intensity of pituitary downregulation. METHODS: Group I (n = 27) received 3.75 mg of the GnRH agonist triptorelin acetate depot, group II (n = 54) was given 0.1 mg triptorelin acetate daily, followed by ovarian stimulation with recombinant FSH. RESULTS: After downregulation serum LH and FSH levels were significantly lower in group I. Patients of group I needed significantly higher FSH doses to achieve comparable levels of serum estradiol and preovulatory follicles. The number of retrieved oocytes and transferable embryos was lower in group I. CONCLUSION: Patients with profound endogenous LH suppression by depot GnRH agonists show higher FSH stimulation dose requirements and lower oocyte number and fertilization rate, indicating a need for minimal LH activity in folliculogenesis and oocyte development.

Adult↗
PubMed2006

Can serum Inhibin B and FSH levels, testicular histology and volume predict the outcome of testicular sperm extraction in patients with non-obstructive azoospermia?

INTRODUCTION: In our study, we evaluated the diagnostic accuracy of serum follicle stimulating hormone (FSH), Inhibin B, testicular volumes and distribution of testicular sperm extraction (TESE) outcome according to the histological diagnosis in men with non-obstructive azoospermia. MATERIALS AND METHODS: Between February 2001 and April 2002, 66 men presenting with infertility of at least 1 year were found to have non-obstructive azoospermia. Serum FSH and Inhibin B levels, testicular volumes and pathological analysis were reviewed retrospectively using medical records of these patients. RESULTS: Of 66 patients, 52 were enrolled into the study and sperm extraction was successful in 31 of 52 patients (59.6%). There was no statistically significant difference between the patients who had successful and unsuccessful TESE in terms of mean serum Inhibin B, FSH levels and testicular volumes (P>0.05). The area under ROC analysis for serum Inhibin, serum FSH and testicular volume was 0.557, 0.523 and 0.479, respectively. For Inhibin B, the best cut-off value for discriminating between successful and failed TESE at 90% sensitivity was 6.25 with a very low level of specificity (14%) and diagnostic accuracy that was 53.8. CONCLUSION: Besides the controversies about the direct marker role of serum Inhibin B in determination of spermatogenesis, it does not seem to give a clue about the prediction of sperm presence before TESE. Because of the conflicting results in the literature, the potential role of serum Inhibin B as a marker for prediction of sperm presence in testis is yet to be determined.

Adult↗
PubMed1977

Basal and LRH-stimulated secretion of FSH during early pregnancy.

The gonadotropin response to 25 mug of LH/FSH releasing hormone (LRH) intravenously was investigated during the very first weeks of pregnancy. It was found progressively to decrease, and no response in FSH was found for more than 5 weeks. The basal levels of FSH showed the same decreasing tendency, and a few weeks after conception they were often close to the sensitivity limit of the assay. With this report we have continued our description of the changing pituitary responsiveness to LRH from conception to the puerperium. During later stages of pregnancy the plasma levels of FSH were markedly reduced, and the response was inhibited even after 500 mug of LRH intervenously. The return of the response during the puerperium showed a specific pattern with a dissociation of the response in FSH and LH. No such dissociation was found during the period of progressive inhibition during the very first weeks of pregnancy.

Adult↗
PubMed1986

Inhibin and beta type transforming growth factor (TGF beta) have opposite modulating effects on the follicle stimulating hormone (FSH)-induced aromatase activity of cultured rat granulosa cells.

We have recently observed that attomolar concentration of exogenously added TGF beta, a molecule structurally related to inhibin, can stimulate the basal secretion of FSH in a pituitary cell culture. Inhibin purified from porcine follicular fluid antagonizes this activity of TGF beta. To understand further the homeostatic regulatory properties of inhibin and TGF beta we have investigated whether the aromatase activity of ovarian granulosa cells is also subject to intra-ovarian modulation by these peptides. Granulosa cells from immature hypophysectomized diethylstilbestrol-treated rats were cultured for 2 days with androstenedione (10(-7) M) as a substrate, oFSH (2 ng), and different amounts of TGF beta or inhibin. Basal estrogen secretion was negligible and remained unaffected by treatment with purified TGF beta or inhibin (10 ng/ml), whereas treatment with oFSH (2 ng/ml) produced a 100-fold increase in estrogen accumulation. The concurrent application of increasing concentrations (10 pg-10 ng/ml) of TGF beta produced dose-dependent increments in the FSH-stimulated accumulation of estrogen with a ED50 of 0.3 +/- 0.02 ng/ml. On the other hand, concurrent incubation of FSH with inhibin ranging from 10 pg to 10 ng/ml decreases the FSH-mediated estrogen secretion. TGF beta antagonizes the inhibition of inhibin on aromatase activity. These findings suggest that inhibin and TGF beta, two closely related molecules, play novel and opposite roles in modulating the follicular functions.

Androstenedione↗
PubMed1986

Type beta transforming growth factor (TGF-beta) is a potent stimulator of the basal secretion of follicle stimulating hormone (FSH) in a pituitary monolayer system.

In view of striking similarities between TGF-beta and inhibin, we investigated the possibility that TGF-beta might modulate pituitary hormone release in vitro. Long term incubations of beta transforming growth factor (TGF-beta) with rat anterior pituitary cells for 48 hr stimulates the basal secretion of FSH in a dose-dependent manner. The secretion of LH, TSH, GH, ACTH and PRL is not modified by TGF-beta. The minimal effective concentration of TGF-beta is 10 pg/ml (less than 500 attomolar) and is dose dependent over a range from 1 pg to 10 ng/ml. Treatment of cells with TGF-beta for short incubation times (4 hr) in assays similar to that used for hypophysial releasing factors is not effective, indicating that TGF-beta acts through a cellular mechanism distinct from that of LRF. Inhibin-A, recently characterized on the basis of its capacity to specifically inhibit the secretion of FSH in the 48 hr bioassay system inhibits the stimulatory effect of TGF-beta on FSH-release. Analyses of the dose response curves indicate that the interaction occurs in a typical non-competitive manner. The results suggest that a TGF-beta-like molecule, present in follicular fluid, may be responsible for the FSH-releasing activity ("anti-inhibin" activity) observed by us and others during the process of isolating inhibin from follicular fluids. They also suggest an important role for inhibin and the TGF-beta related molecules in modulating pituitary gonadotropin release.

Animals↗
PubMed1989

A stimulatory effect of somatostatin: enhancement of activin A-mediated FSH secretion in rat pituitary cells.

The interaction between somatostatin and activin A was studied in terms of FSH secretion in rat pituitary cells in primary culture. Incubation of pituitary cells with 1 nM activin A for 48 hrs resulted in an increase in FSH release into incubation medium. The effect of activin A was dependent on cell-density and the higher the density, the smaller the stimulatory action of activin A. Somatostatin, by itself, did not affect the FSH secretion. When 100 nM somatostatin was included together with activin A or the cells were pretreated with somatostatin for 2 hrs, the activin A-induced FSH secretion was enhanced. This potentiation effect of somatostatin was inversely dependent on the cell-density. These results indicate that somatostatin enhances, rather than inhibits, the activin A action in pituitary cells.

Activins↗
PubMed1995

Temporary increase of FSH levels in healthy, nulliparous, young women after cessation of low-dose oral contraceptive use.

The effect of modern low-dose oral contraceptives (OCs) on the levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) in young, health, nulligravid women was studied in two independent samples. Elevated FSH levels were seen in former OC users compared with never users regardless of menstrual cycle phase. The increase in FSH levels seemed to peak one year after cessation of OC use. This relationship was still significant after exclusion of women with low progesterone levels. LH levels were significantly higher in former users compared with never users in the first sample, but not in the second sample. The difference in FSH concentrations was very small. Single blood samples were obtained from the subjects at each time point even though it is recognized that gonadotropin secretion is pulsatile. These results must be regarded as preliminary and unconfirmed due to small sample size.

Adult↗
PubMed1985

Effect of serum and 12-O-tetradecanoyl-phorbol-13-acetate on FSH-stimulated conversion of 4-androstene-3,17-dione to oestrogens in cell and organ cultures of suckling mouse ovaries.

The effect of serum and 12-O-tetradecanoylphorbol-13-acetate (TPA) on the FSH-stimulated oestrogen production was studied in both cell and organ cultures. Ovaries were removed from (WB X C57BL/6)F1 mice at 9-days of age, and the conversion of 4-androstene-3,17 -dione to oestrogens was stimulated by the addition of FSH in vitro. Either 10% serum (fetal calf, mouse, rat and horse) or 0.1 microM TPA markedly inhibited the FSH-stimulated oestrogen production by dispersed and cultured ovarian cells. In contrast, neither serum nor TPA influenced the oestrogen production in the organ culture. This suggests that the presence of tissue architecture may prevent the inhibitory effect of serum and TPA on the FSH-stimulated oestrogen production.

Androstenedione↗
PubMed1987

Differential effect of glucocorticoids on synthesis and secretion of luteinizing hormone (LH) and follicle stimulating hormone (FSH).

Our previous work has suggested that glucocorticoid pretreatment suppresses the enhanced responsiveness to GnRH seen in serum LH 12 h after castration. By contrast, serum FSH continues to show the castration-induced hypersensitivity to GnRH. Our attempts to replicate this LH suppression in static pituitary culture in vitro were not successful. This suggested to us the possibility that corticoids in vivo might be preventing castration-induced increases in pituitary GnRH receptor levels. We tested this at 24 h post-castration and, in fact, corticoids did not suppress the increase in GnRH receptors. In addition to the aforementioned effects of corticoids, we have seen that cortisol reverses the castration-induced drop in pituitary FSH content. It does this for 7 days post-castration, even though it no longer has an effect in suppressing serum LH. Thus, our accumulated data reveal that glucocorticoids have a differential effect on LH and FSH synthesis and secretion. Further studies are needed to clarify the site(s) of action of glucocorticoids in gonadotropin secretion and synthesis. Glucocorticoids may well prove to be a key in unlocking the mystery of the mechanism of differential control of regulation of LH and FSH.

Animals↗
PubMed1976

Hormonal regulation of LH stimulation of testosterone production in isolated Leydig cells of immature rats: the effect of hypophysectomy, FSH, and estradiol-17beta.

Testosterone production in isolated Leydig cells from testes of immature and adult rats was stimulated by addition of LH in a dose dependent way. Hypophysectomy of adult rats had no influence on LH-stimulated testosterone production in isolated Leydig cells after 5 days. In contrast hypophysectomy of immature rats resulted after 5 days in an almost complete loss of LH sensitivity of isolated Leydig cells. Daily adminitration of FSH during 5 days starting immediately after hypophysectomy maintained LH responsiveness of isolated Leydig cells of immature rats. Also FSH administration starting on day 5 after hypophysectomy resulted in a restoration of LH responsiveness. Estradiol benzoate, injected simultaneously with FSH, abolished the FSH-induced LH responsiveness.

Animals↗
PubMed1978

Glucocorticoid inhibition of FSH-induced estrogen production in cultured rat granulosa cells.

The effects of glucocorticoids on the steroidogenesis of ovarian granulosa cells were investigated. Cortisol and dexamethasone inhibited the increase in aromatase activity induced by FSH in cultured rat granulosa cells. In the same cultures progesterone production was stimulated to a maximum of 167% of the control level. This differential effect of glucocorticoids on estrogen and progesterone production by the granulosa cells indicates that glucocorticoids exert specific inhibition of the induction of aromatase by FSH and do not cause a general suppression of granulosa cell activity. In contrast to their inhibition of the FSH induction of aromatase enzymes, glucocorticoids did not interfere with the activity of pre-existing aromatase enzymes. In granulosa cells containing full aromatase activity, treatment with cortisol and dexamethasone did not inhibit aromatization of androstenedione to estrogens whereas two known aromatase inhibitors (dihydrotestosterone and 4-androstene-3, 6, 17-trione) were effective. These results indicate that the glucocorticoids exert a selective inhibition of the FSH-induction of aromatase activity in rat granulosa cells by a mechanism other than directly interfering with the aromatization reaction.

Animals↗
PubMed1990

Inhibition of FSH-stimulated cAMP accumulation and progesterone production by mono(2-ethylhexyl) phthalate in rat granulosa cell cultures.

Several phthalate esters are male and female reproductive toxicants in vivo. In the male, mono(2-ethylhexyl) phthalate (MEHP), the active metabolite of di(2-ethylhexyl) phthalate (DEHP), inhibits follicle stimulating hormone (FSH)-stimulated cAMP accumulation in the Sertoli cell in vitro. Since granulosa and Sertoli cells share several structural and functional characteristics, the effect of MEHP on granulosa cell intracellular cAMP accumulation was examined to elucidate a possible mechanism for DEHP reproductive toxicity in females. MEHP (100 microM) reduced FSH-stimulated cAMP accumulation in granulosa cells by 40% after a 24-hr preincubation. Significant inhibition of cAMP accumulation by MEHP occurred by 15 hr and MEHP did not affect the dose of FSH which resulted in half-maximal stimulation. Detailed investigations regarding the mechanism of MEHP inhibition were conducted using cholera toxin, forskolin, and isoproterenol. In contrast to FSH, MEHP did not affect the ability of these compounds to stimulate cAMP accumulation. In addition, a functional endpoint of granulosa cell function, progesterone production, was inhibited in a dose-dependent manner by MEHP. Further experiments will be necessary to determine the significance of these findings to in vivo toxicity, but these experiments describe a specific site of action of MEHP in vitro which may be related to the in vivo female reproductive toxicity of phthalate esters.

Adenosine Triphosphate↗
PubMed1980

Response of plasma LH and FSH to gonadotropin-releasing hormone in pony foals and ovariectomized pony mares.

Plasma FSH and LH response to a synthetic GnRH analog was measured in adult ovariectomized pony mares (OVX) and in pony foals (<70 days of age) during late spring (May-June). FSH and LH responded in a similar fashion (200% increase) in the OVX mare, which is different from other reports for intact mares. There was a greater mean response to a comparable dose of GnRH in the prepubertal foal for both FSH (500%) and LH (900%) than in the OVX mare. There was a positive correlation between age and the maximum FSH response to GnRH in male and female foals. The LH response was positively correlated with age in male foals, but not in females. The response to GnRH in the prepubertal foals was consistent with the previously observed patterns of gonadotropin secretion during this age period.

Journal Article↗
PubMed1982

Plasma levels of LH, FSH, prolactin, oestradiol-17beta and progesterone during natural and induced oestrus in the dairy goat.

The patterns of LH, FSH, prolactin and oestradiol-17beta, before and during natural oestrus, and of progesterone during the following cycle were studied in four French Alpine dairy goats and compared with those obtained after synchronization of oestrus in the same animals. The highest concentration of oestradiol-17beta was measured at the beginning of oestrus and was followed 3 hours later by simultaneous rises of LH, FSH and prolactin. A second FSH peak was observed 48h after the first one. On D(3) (D(0) = day of oestrus) progesterone concentration was over 1 ng/ml. The luteal phase lasted 15 days. Peak concentrations of oestradiol-17beta and progesterone were higher in animals when oestrus was induced. This was attributed to their higher ovulation rate. The second FSH peak was lower, and the interval between oestradiol-17beta peak and gonadotrophin surge longer, than at natural oestrus.

Journal Article↗