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PubMed2005

Antral follicle count and FSH concentration after clomiphene citrate challenge test in the prediction of ovarian response during IVF treatment.

BACKGROUND: We compared: (i) antral follicle count (AFC) in the early follicular phase, after the clomiphene citrate challenge test (CCCT) and before ovarian stimulation following pituitary down-regulation; and (ii) age of women, body mass index, basal and stimulated serum FSH concentrations and AFC in predicting the ovarian response of infertile women aged <40 years with basal FSH <10 IU/l on recruitment in their first IVF cycle. METHODS: Two months prior to the treatment cycle, AFC and basal FSH concentration were determined on day 2-3 of a spontaneous period and on day 10 after CCCT. All women received a standard stimulation regimen. Ovarian response was represented by the number of oocytes, serum estradiol, the duration and dosage of gonadotrophins. RESULTS: There was no significant difference between basal, stimulated and down-regulated AFC. AFC achieved the best predictive value in relation to the number of oocytes, followed by combined FSH concentration (sum of the two FSH concentrations) and age of women. Both basal AFC and combined FSH concentration were predictive factors of serum estradiol concentration, whereas stimulated FSH concentration was predictive of the total dosage of gonadotrophins. CONCLUSION: Combined FSH concentration after CCCT provides additional information in predicting ovarian response.

Adult↗
PubMed1992

Regulation of aromatase activity in FSH-primed rat granulosa cells in vitro by follicle-stimulating hormone and various amounts of human chorionic gonadotrophin.

The influence of various amounts of human chorionic gonadotrophin (HCG), with or without follicle-stimulating hormone (FSH), on aromatase activity, progesterone- and cAMP-accumulation in rat granulosa cells was investigated. Cells were isolated from immature diethylstilbestrol-treated rats and primed for 2 days in vitro with FSH (50 mIU/ml) to give a maximum response of the cells with respect to the induction of aromatase activity. After FSH priming, small amounts of HCG (1-5 mIU/ml) increased aromatase activity during an additional culture period of 24 h, with a maximum of 4- to 5-fold at 5-8 mIU/ml HCG. At higher concentrations of HCG, aromatase activity declined reaching a plateau (1.5-fold stimulation) at 20 mIU/ml HCG. When HCG was combined with FSH (50 mIU/ml) following the priming period, aromatase activity was stimulated in an additive way, reaching a maximum at 4-5 mIU/ml HCG followed by a decline, similar to that seen in the absence of FSH. HCG induced a dose-dependent increase in cAMP with a maximum at 20 mIU/ml. This increase in cAMP was higher when HCG was combined with FSH. Aromatase activity was inhibited by 3-isobutyl-methyl-xanthine and forskolin, both of which induce elevated cAMP levels in the cell. HCG, and HCG in combination with FSH, increased the production of progesterone in a dose-dependent manner until a plateau was reached. In the presence of FSH, this plateau was reached at lower HCG concentrations. Both R5020 and progesterone showed dose-dependent inhibition of aromatase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Relationship of inhibin serum level to bioactive and immunoreactive FSH in oligospermic and azoospermic patients.

The purpose of the study described here was to evaluate the relationship between inhibin (INH) and bioactive FSH (B-FSH) or immunoreactive FSH (I-FSH) in oligoazoospermic patients. To accomplish this, the authors measured serum levels of INH, I-FSH, B-FSH, LH and testosterone (T) in 98 male patients attending the andrology Centre at Malphighi Hospital (Bologna) for infertility workup. On the basis of the mean sperm concentration, patients with sperm output > or = 4 x 10(7) ml-1 (n = 30) formed the control group (group A), whereas oligozoospermic patients were divided arbitrarily into three groups. Sperm concentrations for these groups ranged as follows: B, 2-4 x 10(7) ml-1 (n = 14); C, 5 x 10(6)-2 x 10(7) ml-1 (n = 18); D, < 5 x 10(6) ml-1 (n = 17). In addition, the authors studied a group of patients with possible non-obstructive azoospermia (n = 19, group E), confirmed in 16 of them through testicular biopsy. There were no significant differences in serum levels of LH and T among groups. However, azoospermic patients had a significant reduction of the T/LH ratio. Similarly, B-FSH and B/I-FSH ratios were significantly elevated only in group E. INH serum levels did not show any appreciable changes among groups and in azoospermic patients INH correlated significantly and in a positive manner with I-FSH serum levels and negatively with B/I-FSH and T/LH ratios. Within the azoospermic patient group no consistent relationship was evident between INH serum concentration and various degrees of spermatogenetic arrest.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

FSH secretory pattern and degree of concordance with LH in amenorrheic, fertile, and postmenopausal women.

Pulsatile secretion of gonadotropin was investigated in amenorrheic patients and in fertile and postmenopausal women to assess both follicle-stimulating hormone (FSH) episodic secretion and its temporal coupling with luteinizing hormone (LH). Three groups of amenorrheic patients were studied: hyperandrogenic (n = 20), hypogonadotropic (n = 51), and normogonadotropic (n = 31). Nineteen fertile women (during the follicular and luteal phases of the cycle) and sixteen postmenopausal women were investigated as reference groups. All subjects demonstrated the presence of a distinct pulsatile pattern with LH and FSH pulses/4 h as follows: hyperandrogenic 3.95 +/- 0.26 and 3.85 +/- 0.2, hypogonadotropic 3.76 +/- 0.26 and 3.9 +/- 0.16, normogonadotropic 3.5 +/- 0.2 and 3.9 +/- 0.17 LH and FSH pulses/4 h, respectively (means +/- SE). Normal controls showed 4.1 +/- 0.2 and 3.1 +/- 0.2 pulses/4 h for LH (P < 0.05) and 3.2 +/- 0.1 and 3.6 +/- 0.3 pulses/4 h for FSH, during follicular and luteal phases, respectively. Postmenopausal women showed 3.6 +/- 0.2 and 3.0 +/- 0.3 pulses/4 h for LH and FSH, respectively. Specific concordance (SC) index demonstrated that LH and FSH were significantly and simultaneously secreted in all groups. Conversely, LH and FSH were not temporally related during the luteal phase. In conclusion, we report a distinct FSH episodic secretion and its temporal linkage with LH pulses irrespective of plasma concentrations of gonadal steroids in secondary amenorrhea.

Activity Cycles↗
PubMed1983

Pattern of reproductive hormone secretion and disappearance rates of LH and FSH in senile male rats.

Old Long-Evans male rats (24-33 months of age) do show postcastration rise in serum LH but do not have postcastration LH rise in the pituitary both as expressed in content and concentration. The serum LH levels of intact and castrated rats of old age show a tendency of decrease, though not to the level of statistical significance. The pituitary FSH content and concentration of intact old rats are not different from those of young adults (3.5-5 months of age), whereas serum FSH level of intact old male rats is significantly higher than that of intact young adults. There is a postcastration rise in the pituitary FSH content as well as concentration and serum FSH level in both age-groups. The half-lives of endogenous and exogenous LH and FSH are not different between old male rats (24- to 31-month-old) and young adults (3- to 5-month-old). Blood testosterone levels begin to decline between the age of 12 and 18 months and remained low from 18 months of age on. These results indicate: (1) deficiencies in the LH regulatory mechanism in response to removal of gonadal steroids are easier to manifest than those of FSH control mechanism in old age in male rats; (2) the ability of clearing circulating LH and FSH of old male rats is not different from that o young adult males, if their molecular sizes are similar, and (3) high serum FSH level of old male rats is not due to prolonged half-life in the circulation.

Aging↗
PubMed1990

Role of midcycle FSH surge in follicular development.

The present study was undertaken to examine the importance of the proestrous surge of FSH for follicular development during the following cycles in the rat. The midcycle FSH surges were blocked in several consecutive cycles (1-5) by injecting proestrous rats with pentobarbital. The rats were sacrificed on the day of proestrus following the appropriate number of blocked FSH surges and their ovaries were removed for either direct measurements or for histological workout. The number and diameter of follicles were determined in the excised ovaries. Two or three cycles of barbiturate treatment reduced the number and diameter of the follicles. No large follicles (greater than 0.4 mm) were observed in the ovaries of rats in which four or five gonadotropin surges were blocked. A repeat experiment with concomitant supplementary hCG administration yielded the same results. Addition of exogenous FSH canceled the effect of pentobarbital. The cohort observed on ovaries after four cycles of treatment with pentobarbital and FSH resembled that observed in control rats. Histological measurements supported the results obtained with fresh ovaries. It is therefore suggested that in the third cycle preceding the ovulatory one, the midcycle FSH surge determines which follicles will be able to adequately develop in the following three cycles. In the cycle preceding the ovulatory one, the midcycle FSH peak 'rescues' a group of follicles and prepares them for a proper response to the FSH elevation taking place at the beginning of the subsequent ovulatory cycle. This process allows the selection of the dominant follicles which will respond by ovulation to the ensuing LH peak.

Animals↗
PubMed2006

FSH regulates acetycholine production by ovarian granulosa cells.

BACKGROUND: It has been previously shown that cultured granulosa cells (GCs) derived from human ovarian preovulatory follicles contain choline acetyltransferase (ChAT), the enzyme responsible for acetylcholine (ACh) synthesis. They also produce ACh and express functional muscarinic ACh receptors. ACh can act on GCs to increase proliferation, disrupt gap junctional communication, alter intracellular calcium levels, as well as expression of transcription factors, suggesting an unrecognized role of ACh in GC function. To gain further insights into the possible role of ACh in the ovary, we examined ChAT expression in the gland before and after birth, as well as in adults, and studied the regulation of ACh production by FSH. METHODS: ChAT immunohistochemistry was performed using ovarian samples of different species and ages (embryonic, postnatal and adult rats and mice, including embryonic ovaries from mice null for ChAT, neonatal and adult rhesus monkeys and adult humans). ACh was measured by HPLC and/or a fluorescence based method in rat ovaries and in a FSH receptor-expressing cell line (rat GFSHR-17) cultured with or without FSH. RESULTS: In adult rat, as well as in all other species, ovarian ChAT immunoreactivity is associated with GCs of antral follicles, but not with other structures, indicating that GCs are the only ovarian source of ACh. Indeed ACh was clearly detected in adult rat ovaries by two methods. ChAT immunoreactivity is absent from embryonic and/or neonatal ovaries (mouse/rat and monkey) and ovarian development in embryonic mice null for ChAT appears normal, suggesting that ACh is not involved in ovarian or follicular formation. Since ChAT immunoreactivity is present in GCs of large follicles and since the degree of the ChAT immunoreactivity increases as antral follicles grow, we tested whether ACh production is stimulated by FSH. Rat GFSHR-17 cells that stably express the FSH receptor, respond to FSH with an increase in ACh production. CONCLUSION: ACh and ChAT are present in GCs of growing follicles and FSH, the major driving force of follicular growth, stimulates ACh production. Since ACh stimulates proliferation and differentiation processes in cultured GCs, we suggest that ACh may act in the growing ovarian follicle as a local mediator of some of the actions ascribed to FSH.

Acetylcholine↗
PubMed1999

Inverse relationship between serum inhibin B and FSH levels in prepubertal boys with cryptorchidism.

To investigate the gonadal control of FSH secretion in prepuberty, we studied the relationship between circulating inhibin B and FSH levels in 16 prepubertal boys with cryptorchidism (age range, 1-8 y). The effect of Leydig cell stimulation on the secretion of inhibin B, sex steroids, and FSH was investigated in nine boys who were given human chorionic gonadotropin (hCG) treatment. In these boys, serum inhibin B, testosterone, estradiol, and gonadotropin levels were measured before and on the fourth day of the last (third) hCG injection, given at 1-wk intervals. Except for one boy with both high inhibin B and FSH concentrations, basal serum levels of these hormones correlated negatively (r(s) = -0.79, n = 15, p < 0.005). This inverse relationship remained significant in the subgroup of boys younger than 2 y of age (r(s) = -0.84, n = 11, p = 0.008) who also had greater variance of serum FSH concentrations than 14 control boys of similar age with normally located testes (p < 0.01). hCG stimulation increased serum testosterone and suppressed serum FSH concentrations in each boy (n = 9, p < 0.005). In the four oldest subjects, the serum inhibin B level increased from the mean of 91 to 135 pg/mL (p < 0.05). These findings suggest that inhibin B regulates FSH secretion in early childhood. Moreover, the hCG-induced suppression of FSH secretion was probably mediated by sex steroids rather than by inhibin B. Finally, the increase in serum inhibin B concentration during the hCG treatment was likely to be indirect via Leydig cell-Sertoli cell or Sertoli cell-germ cell interaction(s).

Child↗
PubMed2001

The functional significance of FSH in spermatogenesis and the control of its secretion in male primates.

The aim of this review is to provide an integrative analysis of the role of FSH in the control of testicular function in higher primates, including man. Attention is focused on the action of FSH during neonatal development, puberty, and adulthood. Whether FSH is the major determinant of the adult complement of Sertoli cells and whether FSH is obligatory for the initiation, maintenance, and restoration of spermatogenesis is evaluated. The mechanism whereby the circulating concentration of FSH regulates spermatogonial proliferation to dictate the sperm production rate under physiological conditions in the adult is discussed in detail. Inhibin B is the major component of the testicular negative feedback signal governing FSH beta gene expression and FSH secretion, and the evidence for this view is presented. The review concludes with the presentation of a model for the operation of the FSH-inhibin B feedback control system regulating sperm production postpubertally in monkey and man, and with speculation on issues of clinical interest.

Animals↗
PubMed2002

FSH and TGF-beta superfamily members regulate granulosa cell connective tissue growth factor gene expression in vitro and in vivo.

Connective tissue growth factor (CTGF) is a heparin-binding growth factor implicated in diverse epithelial cell types as a paracrine regulator of mitosis, angiogenesis, cellular taxis, and remodeling of the extracellular matrix. To understand the possible roles of CTGF in the ovarian paracrine system, we studied CTGF gene expression by granulosa cells in relation to their stage of cellular differentiation using both in vitro and in vivo methodologies. Untreated monolayer granulosa cell cultures from immature rats abundantly expressed the approximately 2.5-kb CTGF mRNA transcript (determined by Northern analysis), but had low levels of aromatase activity (an index of granulosa cell differentiation). Treatment for 48 h with FSH (0.1-10 ng/ml) dose-dependently inhibited (>or=50%) CTGF mRNA expression, but enhanced aromatase enzyme activity. This in vitro observation of CTGF mRNA down-regulation coinciding with FSH-induced granulosa cell maturation is substantiated by studies of in vivo ovarian CTGF expression in FSHbeta knockout mice. Northern blot and in situ hybridization analyses demonstrate high levels of CTGF expression in the granulosa cells of preantral follicles blocked from further development by the absence of FSH. The action of FSH (10 ng/ml) was mimicked in vitro by 8-bromo-cAMP (1.0 mM) and was augmented by the additional presence of androgen (1 micro M 5alpha-dihydrotestosterone), consistent with mediation by intracellular cAMP. Conversely, treatment of granulosa cell cultures with TGFbeta1 (0.1-10 ng/ml) dose-dependently increased CTGF mRNA levels up to 12-fold at a dose of 10 ng/ml, without affecting aromatase activity. Cotreatment with FSH (0.1-10 ng/ml) dose-dependently suppressed the stimulatory action of TGFbeta1 (10 ng/ml) on CTGF mRNA, but substantially enhanced aromatase activity beyond levels induced by FSH alone. Importantly, other TGFbeta superfamily members known to be produced in the ovary (growth/differentiation factor-9 and activin A; 10 ng/ml) stimulated granulosa cell CTGF mRNA in a similar fashion as TGFbeta1 (10 ng/ml), and this was also inhibited by FSH (10 ng/ml). These data show that granulosa cell CTGF gene expression is inversely related to the stage of granulosa cell differentiation, being directly inhibited by FSH via cAMP-mediated signaling. CTGF mRNA abundance in nondifferentiated granulosa cells is up-regulated in vitro by TGFbeta1, growth/differentiation factor-9, and activin, suggesting paracrine roles for these growth/differentiation factors in the regulation of CTGF synthesis in mammalian ovaries.

Activins↗
PubMed1977

Acute and chronic elevations in serum levels of FSH after unilateral ovariectomy in the cyclic hamster.

During the normal 4-day estrous cycle of the hamster, 12.0 +/- 0.4 (n = 34) ova were shed by the paired ovaries on Day 1. When unilateral ovariectomy (ULO) was performed at 0900 h on any one of the first 3 days of the cycle, approximately the same number of ova were released from the remaining ovary on Day 1 of the ensuing postoperative cycle (compensatory ovulation), except after ULO on Day 4. In view of these results, the principal aim of the present study was to determine if ULO affected acute (24 h postoperative period) and chronic (postoperative cycles) alterations in serum levels of immunoreactive FSH. Multiple bleedings were obtained by cardiac puncture without anesthesia. The acute alteration in FSH levels was first examined at 24-h intervals following ULO at 0930 h on any one day of the cycle, and significant elevations in these levels were found 24 h postoperatively in all but Day-2 hemicastrates. Several experiments were then performed to determine the time-sequence for this 24-h response to ULO. The serum level of FSH was measured at 4-h intervals during the remainder of the cycle in which ULO was done at 0900 h on any one day. The results demonstrated that an acute but transient increase (approximately 100 ng FSH/ml serum) occurred either 7 h or 11 h postoperatively in all the hemicastrates. These transient elevations prior to Day 4 were interpreted to be possible causative factors for the subsequent compensatory ovulation. That they were not the sole cause was evident from the results of another experiment, where compensatory ovulation occurred after ULO at 0030 h on Day 4 (but to a reduced degree; 9.0 +/- 0.6 ova), although serum levels of FSH were not acutely altered. The capability of the remaining ovary to undergo compensatory ovulation after ULO on Day 4 was lost between 0300 h and 0230 h (6.7 +/- 0.8 ova). The serum profile of FSH during the second postoperative cycle after ULO showed a prolonged elevation of FSH levels during the first two days of the cycle compared to the intact estrous cycle. Specifically, the level of FSH gradually declined to 400 ng/ml by 2000 h on Day 1 of the intact (preoperative) cycle but did ont reach this concentration until 2000 h on Day 2 of the postoperative cycle. It is suggested that the prolonged elevated levels of FSH in chronic hemicastrates effect development of a greater number of follicles in the early growth stages in the remaining ovary than the number of follicles per ovary that would otherwise develop in the intact hamster.

Animals↗
PubMed1976

Effect of neuraminidase treatment on the biological activity of highly purified ovine FSH and LH in hypophysectomized immature male and female rats.

Highly purified ovine FSH and LH were treated with neuraminidase to remove sialic acid and the desialylated derivatives were examined for biological activity in hypophysectomized immature male and female rats. The male rats were hypophysectomized at 22 days of age and beginning on day 25 were injected sc twice daily for 4 days with native or neuraminidase-treated FSH (total dose, 15 or 60 mug) or LH (12 mug). The ventral prostates, seminal vesicles, and testes were then removed and weighed, and serum testosterone levels were measured by radioimmunoassay. The female rats were hypophysectomized on day 28 and beginning on day 35 were injected sc twice daily for 4 days with native or neuraminidase-treated FSH (8 mug) or saline. On the morning of day 39, the rats were given an ovulating dose of gonadotropin (8 mug native or neuraminidase-treated FSH, or 1.28 mug native or neuraminidase-treated LH) or 1.0 ml saline iv via tail vein. Twenty-four hours later ova were counted in the oviducts the ovaries were weighed, and serum levels of progesterone and 20alpha-dihydroprogesterone were determined by radioimmunoassay. Treatment of ovine LH with neuraminidase did not diminish the ability of this hormone to increase prostate and testes weights and serum testosterone levels. Desialylation also did not decrease the ability of LH to induce ovulation. Although native ovine FSH significantly increased the weights of the ventral prostate, seminal vesicles, and testes, and elevated plasma testosterone levels, the desialylated derivative was essentially inactive. Neuraminidase treatment also eliminated the ability of ovine FSH to increase ovarian weight, to induce ovulation, and to elevate serum progesterone and 20alpha-dihydroprogesterone. These results indicate that the LH-like activity of ovine FSH is an intrinsic property of the FSH molecule.

Animals↗
PubMed1976

Induction of follicle-stimulating hormone (FSH) receptors in rat ovaries by estrogen priming.

Estrogen pretreatment of hypophysectomized immature rats stimulated granulosa cell proliferation and enhanced FSH binding to the ovary in vivo. The present studies were undertaken to ascertain whether estrogen pretreatment altered the number of specific FSH receptor sites per ovarian cell, resulting in increased FSH binding. Cell suspensions were prepared from the ovaries of groups of rats pretreated with graded doses of 17beta-estradiol. The isolated cells contained specific FSH receptors with high affinity for FSH. The results of these studies clearly showed that the number of specific FSH receptors per ovarian cell was unaffected by pretreatment with graded doses of 17beta-estradiol or with diethylstilbestrol. The enhanced in vivo FSH binding was solely the result of estrogen-induced proliferation of granulosa cells with a fixed number of specific FSH receptors per cell.

Animals↗
PubMed1993

Insulin-like growth factors (IGFs) block FSH-induced proteolysis of IGF-binding protein-5 (BP-5) in cultured rat granulosa cells.

Rat granulosa cells (GC), in vitro, express IGFBPs under the influence of both FSH and IGF-I. The major IGFBP produced by GC is a 28-29 K IGFBP, presumed to be IGFBP-5. When GC-conditioned medium (GC-CM) was assessed by Western Ligand Blotting (WLB), FSH appeared to decrease IGFBP-5, whereas IGF-I appeared to increase IGFBP-5 and to partially block the effects of FSH treatment. When GC-CM from FSH-treated cells was incubated with pure IGFBP-4 and IGFBP-5, the amount of IGFBP-5 (measurable by WLB) was decreased. Similarly, when GC-CM from FSH-treated cells was incubated with iodinated IGFBP-4 and IGFBP-5, IGFBP-5 (but not IGFBP-4) was proteolyzed into fragments of approximately 18 and 14 K. The ability of FSH-treated GC-CM to proteolyze IGFBP-5 was reduced by the addition of IGF-I to the reaction mixture. When the IGFBPs in GC-CM were evaluated by affinity crosslinking, GC-CM from control cultures contained one band with an apparent M(r) of approximately 34 K, whereas GC-CM from FSH-treated cultures displayed a decrease in the intensity of the 34 K band, as well as a new band of approximately 24 K. These data suggest that rat GC cells produce an FSH-inducible IGFBP-5 protease activity, and reveal that the ability of this protease to cleave IGFBP-5 is blocked by IGFs.

Animals↗
PubMed1996

Specific immunoneutralization of FSH leads to apoptotic cell death of the pachytene spermatocytes and spermatogonial cells in the rat.

Although requirement for follicle stimulating hormone (FSH) in the initiation of spermatogenesis is well documented, its role in adult spermatogenesis is still debated. In the present communication, we have investigated the effect of specific immunoneutralization of FSH on apoptotic cell death in the testicular germ cells both in immature and adult rats. The germ cells of control animals showed predominantly high molecular weight DNA while the antiserum (a/s) treated group showed DNA fragmentation characteristic of apoptosis. The pattern could be detected within 24 hours of a/s treatment, and became more pronounced after 48 hours. The germ cells were purified from FSH a/s treated rats by centrifugal elutriation and vulnerability of each cell type to undergo apoptosis on FSH neutralization was investigated. The pachytene spermatocytes were found to be most sensitive to absence of FSH, even in the adult animals suggesting the involvement of FSH in spermatogenesis. The in situ analysis of DNA strand breakage following FSH a/s treatment showed fragmentation of the DNA of the pachytene spermatocytes confirming this observation. The in situ analysis also showed that the spermatogonia undergo apoptosis in addition to the pachytene spermatocytes. These data clearly demonstrate the role of FSH in the adult rat spermatogenesis.

Animals↗
PubMed2001

Synergism between FSH and activin in the regulation of proliferating cell nuclear antigen (PCNA) and cyclin D2 expression in rat granulosa cells.

Follicular development is associated with both proliferation and differentiation of granulosa cells under the control of FSH. We show that regulation of genes involved in cellular proliferation by FSH can be functionally separated from the regulation of genes involved in granulosa cell differentiation by synergistic actions of activin and T. Incubation of undifferentiated rat granulosa cells with FSH, forskolin, activin-A, or T alone did not influence either the expression of the proliferation-associated genes cyclin D2 and proliferating cell nuclear antigen or the differentiation-associated genes P450 aromatase, LH receptor, P450 cholesterol side-chain cleavage enzyme, and 3 beta-hydroxysteroid dehydrogenase. However, when granulosa cells were stimulated with either FSH or forskolin in the presence of activin-A, significant increases (P < 0.05) were observed for cyclin D2 and proliferating cell nuclear antigen at both the mRNA and protein levels as well as mRNAs for P450 aromatase, LH receptor, P450 cholesterol side-chain cleavage enzyme and 3 beta-hydroxysteroid dehydrogenase. Although T synergized with FSH to increase the expression of mRNAs for P450 aromatase, LH receptor, P450 cholesterol side-chain cleavage enzyme, and 3 beta-hydroxysteroid dehydrogenase, it did not interact with FSH to increase the expression of mRNAs for cyclin D2 and proliferating cell nuclear antigen. The differences in the actions of activin and T could provide a cellular mechanism by which FSH-regulated granulosa cell proliferation could be functionally separated from FSH-regulated granulosa cell differentiation.

Activins↗
PubMed2002

Hypersecretion of FSH in infant boys and girls born small for gestational age.

Prenatal growth restraint, as reflected in a low birthweight for gestational age, is a risk factor for postpubertal FSH hypersecretion and for reduced gonadal size. The ontogeny of the low-birthweight effect on the FSH-inhibin B feedback loop is unknown. Infancy is an episode of choice to study the possibility of an early low-birthweight effect on the FSH-inhibin B loop because this phase is characterized by high activity within the gonadal axis. We assessed serum concentrations of FSH and inhibin B in 46 infants [26 girls and 20 boys; mean age, 4 months; range, 3-6 months; 17 appropriate for gestational age (AGA), 29 small for gestational age (SGA); mean birthweight, 3.2 kg for AGA vs. 2.3 kg for SGA], together with circulating levels of LH, E2, and free androgen index. In SGA girls and boys, serum FSH levels were 2- and 4-fold higher (P < 0.001), respectively, than in AGA controls of the same gender (7.3 +/- 0.9 vs. 3.8 +/- 0.4 IU/ml and 2.9 +/- 0.5 vs. 0.7 +/- 0.2 IU/ml). Serum LH, inhibin B, and free androgen index/E2 concentrations were similar in AGA and SGA infants. In conclusion, prenatal growth restraint was found to be followed by elevated serum FSH concentrations in infant girls and boys. SGA infants seem to need an augmented FSH drive to fulfill inhibin B requirements on the afferent side of the feedback loop. The late-endocrine correlates of early growth restraint are herewith extended to include the main axis of reproduction in both genders. It remains to be studied whether FSH hypersecretion in infancy is a marker of subsequent subfertility.

Cohort Studies↗
PubMed1975

[LH and FSH responses to synthetic LH-RH in various estradiol levels of anovulatory women (author's transl)].

Synthetic LH releasing hormone (LH-RH) is effective in increasing both serum LH and FSH in humans. Therefore, LH-RH is used to clarify the function of the hypothalamic pituitary ovarian axis in adult women. Variations in response to synthetic LH-RH during different phases of the menstrual cycle are known. These variations may be due to changes in the ovarian secretion of sex streoid hormones during the menstrual cycle. In the present study, effects of serum estradiol (Ed) on pituitary gonadotropin response to synthetic LH-RH were studied in 55 subjects without ovulation. Serum levels of LH, FSH and Ed were determined before and at 30 min after intramuscular administration of 100 mug LH-RH. LH and FSH levels in the serum were measured by the double antibody method of radioimmunoassay. Ed levels were determined by the radioimmunoassay method of T. Makino, using the antiserum against Ed-6-oxime-BSA donated by Dr. T. Makino and applied to the microcolumn of sephadex LH 20. Preliminary evidence about Ed levels during the normal menstrual cycle and in anovulatory women suggested that an Ed level under 30 pg/ml indicates the presence of a small amount of Ed. Therefore, 55 patients were divided into 2 groups; the low Ed group that showed low basal Ed levels (under 30 pg/ml) and the Ed normal group that showed normal basal Ed levels (over 30 pg/ml). Pituitary gonadotropin responses to synthetic LH-RH were studied in these two groups. No statistical difference was shown between the two groups studied for basal LH level and FSH level. After LH-RH injection in the Ed normal group, serum LH level was significantly higher and serum FSH level was significantly lower than that in the low Ed group. Then, in order to clarify the difference in two groups, the ratio of LH to FSH (LH/FSH) before and after administration of LH-RH was examined. The ratio in the Ed normal group was significantly higher than one in the low Ed group before and after administration of LH-RH. Moreover, the percentage increase of the ratio was significantly larger in the Ed normal group than that in the low Ed group. A positive correlation (r=0.4228, p less than 0.01) was found between LH/FSH following administration of LH-RH and circulating the Ed level. These results suggest that the response of pituitary gonadotropins to LH-RH is changed by serum Ed and that serum Ed causes a differential release of LH and FSH in response to LH-RH. The data seem to demonstrate that LH-RH and serum Ed show a complex interplay in releasing LH and FSH.

Adult↗