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PubMed1988

Inhibin secretion by the sheep ovary during the luteal and follicular phases of the oestrous cycle and following stimulation with FSH.

The secretion of oestradiol and inhibin were measured during the follicular and luteal phase of the cycle by a sensitive bioassay using sheep pituitary cells in culture in four ewes in which the left ovary had been autotransplanted to the neck. On day 12 of the cycle, premature luteal regression was induced with an injection of 100 micrograms cloprostenol (prostaglandin F2 alpha analogue; PG) and ovarian venous blood was collected every 4 h for 72 h. These same four ewes were infused in the ensuing cycle with NIH-oFSH-S14 at 10 micrograms/h for 48 h immediately after an injection of PG and sampled as above. During the luteal phase (-2 h before PG) both in the control and FSH-infused cycles the inhibin secretion rate (SR) was 27-45 units/min. After PG injection, the inhibin SR declined with time to reach 3.6-5 units/min at the onset of the LH surge (60 h after PG) in the control cycle. In contrast, in the following cycle infusion of FSH after PG injection caused a slight increase in the inhibin SR which then remained raised at 42-50 units/min for up to 60 h after PG. In the late follicular phase the oestradiol SR was greater in the FSH-infused than in the control cycles, indicating multiple follicular development. In the FSH-infused cycle the preovulatory surges of LH and FSH were markedly attenuated. These data demonstrate that (1) inhibin SR is high during the luteal phase suggesting that the sheep corpus luteum secretes inhibin, (2) in the control cycle inhibin SR declines during follicular maturation at a time when oestradiol SR is increasing but FSH levels are decreasing, and (3) exogenously administered FSH stimulates the secretion of inhibin from the ovary during the follicular phase.

Animals↗
PubMed1989

Changes in the plasma concentrations of inhibin throughout the normal sheep oestrous cycle and after the infusion of FSH.

A radioimmunoassay for inhibin was developed using a peptide containing the 1-26 amino acid sequence of the N-terminus of the alpha-chain of 32 kDa porcine inhibin as immunogen, and 125I-labelled tracer. Evaluation of this assay using Sephadex column chromatography, chromatoelectrophoresis and immunoblotting confirmed that it measured all forms of inhibin present in sheep follicular fluid and was suitable for measurement of inhibin in sheep plasma. There was no evidence of the presence of free alpha-subunit in either sheep follicular fluid or ovarian vein plasma. The concentration of inhibin in jugular plasma throughout the follicular and luteal phases of four ewes with ovarian autotransplants was measured. The ovarian secretion of inhibin and oestradiol were also measured simultaneously throughout the follicular phase in a spontaneous cycle and after infusion of NIH-oFSH-S14 at 10 micrograms/h for 48 h following premature luteal regression induced by prostaglandin. The results showed: (1) no change in the peripheral concentration of inhibin throughout the cycle except an increase related to the periovulatory increase in FSH and LH. (2) Following luteal regression, the concentration of FSH fell as the secretion rate of oestradiol increased. During this time there was no significant change in the peripheral concentration of inhibin or ovarian inhibin secretion rate. (3) Following the infusion of FSH there was a marked increase in the concentration of inhibin in both ovarian and peripheral plasma and an increase in ovarian inhibin secretion rate. (4) The calculated metabolic clearance rate of inhibin, 20.3 ml/min, is similar to that of FSH. We conclude that in the ewe the ovarian inhibin secretion rate is stimulated by FSH and, although inhibin may modulate the basal secretion of FSH, a change in its secretion does not account for the fall in FSH which occurs during the follicular phase of the sheep oestrous cycle.

Animals↗
PubMed1989

Inhibitory effects of corticotrophin-releasing factor and beta-endorphin on LH and FSH secretion in the lactating rat.

The roles of corticotrophin-releasing factor (CRF) and beta-endorphin in the suppression of LH and FSH secretion during lactation were investigated using ovariectomized lactating rats separated from their litters overnight. Within 1 h of returning the pups to their mothers a marked fall in plasma LH concentration and a large increase in plasma prolactin were noted. However, resuckling caused no significant change in plasma concentration of FSH until 12 h after the return of the litter but a significant decline occurred thereafter. Twenty-four hours after removal of the litter, a single i.v. injection of 200 microliters anti-LHRH serum caused similar changes in plasma concentrations of LH and FSH observed in nursing rats during suckling. These results suggest that the suckling stimulus itself is responsible for the suppression of LH as well as FSH, via inhibition of the secretion of LHRH. Twenty-four hours after removal of the litter, a single intracerebroventricular (i.c.v.) injection of either 10 micrograms CRF or beta-endorphin resulted in a rapid decrease in plasma LH. Only beta-endorphin caused a marked increase in plasma levels of prolactin within 1 h whereas FSH was less affected by either hormone. Repeated i.c.v. administration of 10 micrograms CRF or beta-endorphin at 6-h intervals caused a prolonged inhibition of LH as well as FSH secretion during 48 h, with beta-endorphin being less effective than CRF. These results demonstrate that the suckling stimulus alone suppressed the secretion of both LH and FSH, and suggest that this effect may be mediated by the inhibition of LHRH secretion from the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

FSH causes a time-dependent stimulation of preovulatory follicle growth in the absence of pulsatile LH secretion in ewes chronically treated with gonadotrophin-releasing hormone agonist.

The study investigated the relationship between the plasma concentration of FSH and the stimulation of preovulatory follicle growth in vivo in ewes chronically treated with the gonadotrophin-releasing hormone (GnRH) agonist buserelin (HOE 766). Welsh Mountain ewes with regular oestrous cycles were treated for 6 weeks with two discs implants placed s.c., each containing 5 mg of the agonist in a matrix of polyhydroxybutyric acid. Treatment with the agonist for 35 days produced a sustained suppression of the plasma concentration of FSH, stopped the pulsatile release of LH and prevented follicular development beyond 2.5 mm diameter. There was no difference between the total number of follicles greater than 1.0 mm diameter present in the ovaries of GnRH agonist-treated ewes and day 8 luteal phase control ewes. During the sixth week of agonist treatment ewes were infused with ovine FSH (6 micrograms NIADDK-oFSH-16/h) in the presence of only basal concentrations of LH. After 24, 48, 72 or 120 h of FSH infusion, the mean number of follicles greater than 1.0 mm diameters per ewe was not significantly different between treated and control animals. Infusion of FSH caused a time-dependent increase in (1) the number of follicles per ovary greater than 2.5 mm, (2) the mean diameter of these follicles and (3) the proportion of the large follicles which could be classified as oestrogenic (greater than 3.7 nmol oestradiol/follicle per h in vitro). Injection of human chorionic gonadotrophin (750 IU i.m.) after 120 h of FSH infusion caused the majority of these large follicles to ovulate and form apparently normal corpora lutea. These results indicate that, in the absence of pulsatile LH, FSH stimulates the growth of normal large oestrogenic follicles which, when stimulated, ovulate to produce viable corpora lutea.

Animals↗
PubMed1991

The self-priming action of LHRH is under negative FSH control through a factor released by the ovary: observations in female rats in vivo.

Female rats were treated with Metrodin (highly purified urinary FSH from menopausal women) or saline during the oestrous cycle. On the day of pro-oestrus they were anaesthesized with phenobarbital and received four repetitive LHRH injections 1 h apart. This treatment with FSH suppressed the unprimed LH response to the first LHRH injection. During the subsequent injections the maximal LHRH self-priming was delayed by 3 h till the fourth LHRH stimulation. At this time, LH release in response to LHRH was equally as high as shown in the saline controls after the second LHRH injection. Ovariectomized rats did not show the self-priming effect and FSH treatment was ineffective in suppressing LHRH-induced LH release. Administration of FSH followed by an additional 4- or 24-h period before LHRH stimulation were equally effective in suppressing the unprimed LH release and delaying (up to 3 h) the maximal priming of LH release by LHRH. Even 4-20-fold increased amounts of LHRH did not affect the suppressed unprimed release of LH after FSH treatment. Treatment with FSH did not change oestradiol and progesterone levels. It was concluded that FSH treatment suppresses the unprimed LHRH-induced LH release and delays maximal LHRH self-priming by enhancing the release of an ovarian factor.

Animals↗
PubMed1993

The ability of steroid-free bovine follicular fluid to suppress FSH secretion and delay ovulation persists in heifers actively immunized against inhibin.

Previous reports indicate that administration of steroid-free bovine follicular fluid (bFF) to intact heifers suppresses plasma FSH levels and delays the timing of ovulation. In addition, cessation of bFF treatment is associated with a rebound hypersecretion of FSH. To test the hypothesis that these effects of bFF are mediated by inhibin, we have compared the responses to bFF treatment in heifers actively immunized against the N-terminal sequence of inhibin alpha subunit (bI alpha(1-29)Tyr30-ovalbumin) with those in ovalbumin-immunized controls. Oestrous cycles were synchronized, and inhibin-immune (n = 10) and control (n = 10) heifers were subdivided into two groups which received either 5 ml bFF (n = 5) or 5 ml bovine serum (n = 5) every 4 h for a 60 h period starting 8 h before prostaglandin (PG)-induced luteolysis. Blood was withdrawn every 4 h for 10 days starting 30 h before luteolysis and ovaries were examined daily by ultrasonography. Overall, mean ovulation rate in bI alpha(1-29)Tyr30-immunized heifers was 44% higher (P < 0.02) than in controls. Inhibin antibody titres tested in bI alpha(1-29)Tyr30-immunized heifers before (19 +/- 3%), during (19 +/- 3%) and after (20 +/- 3%) bFF treatment did not differ. In the pretreatment period (i.e. mid-luteal phase), plasma FSH levels were 32% (P < 0.05) higher in inhibin-immunized than in control heifers. During administration of bFF to control heifers, plasma FSH was suppressed to a level 40% lower than in serum-treated heifers (P < 0.02). Unexpectedly, bFF suppressed FSH to a similar extent in inhibin-immunized heifers (37% lower than in the serum-treated group; P < 0.025). Similarly, a post-bFF rebound hypersecretion of FSH was observed in both control (P < 0.05) and inhibin-immunized (P < 0.05) heifers, although the FSH rebound lasted about 24 h longer in the latter group (P < 0.001). The timing of the preovulatory LH surge in control (86 +/- 7 h post-PG) and immunized (81 +/- 6 h post-PG) groups treated with serum was similar as was the timing of the preovulatory rise in plasma oestradiol and the subsequent rise in plasma progesterone. However, bFF treatment delayed (P < 0.001) the preovulatory surges of LH and oestradiol and the subsequent rise in plasma progesterone to a similar extent (> 4 days) in both control and inhibin-immunized groups.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

The antiprogestin RU486 dissociates LH and FSH secretion in male rats: evidence for direct action at the pituitary level.

Administration of 4 mg of the antisteroid RU486 over 8 consecutive days to adult male rats dissociated in vivo and in vitro gonadotrophin secretion, increasing FSH and decreasing LH secretion. In subsequent experiments we evaluated the involvement of testicular or adrenal secretory products, as well as hypothalamic LHRH, in the effects of 4 consecutive days of RU486 treatment on the secretion of gonadotrophins. The first day of RU486 injection was designated day 1, subsequent days being numbered consecutively. Groups of rats injected with oil (0.2 ml) or RU486 (4 mg) were: (i) injected s.c. from day 1 to day 4 with the antiandrogen flutamide (10 mg/kg); (ii) bilateral orchidectomized (ORCH) on day 1; and (iii) bilateral adrenalectomized (ADX) on day 1. Controls were given flutamide vehicle or were sham operated. To ascertain whether the secretion of LHRH is involved in the effects of RU486 on gonadotrophin secretion, we measured the LHRH secretion into the pituitary stalk blood vessels at 1100 h on day 5 in oil- or RU486-treated rats. Additional oil- and RU486-treated rats were injected i.p. with 100 ng LHRH at 1000 h on day 5, or s.c. with 1 mg LHRH antagonist (LHRH-ANT) at 1000 h on days 2 and 4. Controls were given saline. All animals were decapitated at 1100 h on day 5, trunk blood collected and serum stored frozen until FSH, LH and testosterone assays.%While ADX had no effect on FSH and LH secretion in either oil- or RU486-treated rats, the removal of androgen negative feedback with flutamide treatment or by ORCH substantially increased serum levels of FSH and LH in both oil- and RU486-treated rats, and thus annulled the effects of RU486. No differences in pituitary stalk plasma LHRH concentrations were found between oil- and RU486-treated rats. Injection of LHRH increased serum FSH and LH concentrations in oil-treated rats but only, and to a lesser extent, LH concentrations in RU486-treated rats. Treatment with LHRH-ANT decreased serum concentrations of FSH and LH in both oil- and RU486-treated rats. These results suggest that RU486 inhibited LHRH-stimulated LH secretion at the pituitary level, and that FSH secretion increased in response to a reduction in the negative feedback of androgen.

Adrenalectomy↗
PubMed1983

Testosterone effects on mares during synchronization with altrenogest: FSH, LH, estrous duration and pregnancy rate.

Twelve mares fed altrenogest for 14 d were used to study the effects of a single injection of testosterone propionate on concentrations of follicle-stimulating hormone (FSH) during diestrus, and to relate the normal and perturbed patterns of FSH secretion to subsequent estrous characteristics and fertility. Seven of 12 mares received testosterone propionate at 200 micrograms/kg of body weight on d 5 of progestogen feeding. Mares were teased and blood samples were drawn daily; all mares were artificially inseminated at the first estrus after progestogen treatment. Testosterone propionate treatment caused a 50% reduction in concentration of FSH in plasma within 24 h, and this effect persisted through 48 h after injection. Within 4 d after the suppression of FSH secretion, concentrations of FSH rebounded and were significantly elevated compared with control values during the last 4 d of progestogen feeding. Testosterone propionate at this dosage also elicited estrous behavior in five of seven treated mares within 24 h after injection. After withdrawal of progestogen feeding, the interval to onset of estrus, duration of estrus, and magnitude of the luteinizing hormone peak were similar between groups (P greater than .05). Six of seven treated mares and three of five control mares became pregnant to breeding on the first estrus after progestogen treatment. Because manipulation of the normal pattern of FSH secretion during diestrus did not affect estrous characteristics or fertility of the subsequent estrus, such treatment may have potential as a means of synchronizing FSH surges during diestrus in the mare.

Animals↗
PubMed1983

On the negative feedback regulation of gonadotropins in castrate and intact cattle with comparison of two FSH radioimmunoassays.

Two homologous radioimmunoassays for bovine follicle stimulating hormone (bFSH) were utilized in comparing the differential regulation of FSH and luteinizing hormone (LH) in response to ovariectomy or administration of gonadal steroids in cattle. There appeared to be significant LH cross-reactivity in one of the bFSH systems (bFSH-HS-2-17), but not in the other (bFSH-BP3). Concentrations of FSH in plasma measured by these two systems suggested both qualitative and quantitative differences. Following ovariectomy in heifers, LH concentrations in plasma were increased by 7.5 h, while FSH (measured in the bFSH-BP3 system) was not significantly elevated until 18 h. Administration of 200 micrograms of estradiol-17 beta to ovariectomized heifers inhibited levels of FSH in plasma but large doses of testosterone (100 mg), androstenedione (400 mg) and dihydrotestosterone (800 mg) had no effect. Similarly, LH was not affected by the androgens, while estradiol induced LH surges, leading to increased mean LH concentrations. In contrast to the results in heifers, LH concentrations in plasma from steers were inhibited by administration of androgens as well as by estradiol. In steers, FSH (bFSH-BP3) was marginally inhibited by estradiol and not at all by the androgens. Differences in the secretory patterns of FSH and LH also occurred in intact heifers during the estrous cycle. The 72-h period preceding estrus (follicular phase) was characterized by rapidly declining serum progesterone concentrations, followed by concurrent increases in both LH and estradiol. The circulating levels of bFSH (BP3) tended to decline during this interval. Overall, during the estrous cycle, progesterone levels were positively correlated with bFSH-BP3 (r = .37) and negatively correlated with LH (r = -.39). The gonadotropins were not significantly related (r = -.15). These relationships are consistent with the concept that LH controls the final stages of follicular development in cattle and that FSH may exert only a permissive effect.

Androstenedione↗
PubMed1986

Age, dose of FSH and other factors affecting superovulation in Holstein cows.

Effects of age of donor and other factors on superovulation and production of transferable embryos were investigated. Data were obtained on 987 recoveries of embryos performed between November 1980 and June 1984 by Select Embryos, Inc. The 339 Holstein donors ranged in age from 1.8 to 17.8 yr. The effects of age of donor and dose of follicle stimulating hormone (FSH) were examined using regression analysis. For on-farm recoveries, numbers of embryos, rates of fertilization, quality scores of all embryos and numbers of transferable embryos decreased (P less than .01, P less than .001, P less than .05, P less than .01, respectively) with increasing age of donor. For in-clinic recoveries, numbers of embryos plus ova recovered were affected by age of donor, dose of FSH and the interaction of the two (P less than .05). Among older donors, increasing doses of FSH were associated with an increase in the number of ova plus embryos recovered. However, among younger donors, increasing doses of FSH had a negative effect. Numbers of embryos, rates of fertilization and numbers of transferable embryos decreased (P less than .05) with advancing age and increased (P less than .05) with increasing doses of FSH. Greater numbers of ova plus embryos were recovered when treatment with FSH was begun on d 10 or 11 as compared with d 7, 8, 9, 12, 13 or 14 (P less than .001). It was concluded that an increase in age of donor had a negative influence on the success of superovulation and the production of transferable embryos, and that the response to FSH was affected by age of donor.

Animals↗
PubMed1983

Effects of FSH, isoproterenol, and cyclic AMP on the production of lactate and pyruvate by cultured Sertoli cells.

We have examined the hormonal regulation of the secretion of lactate and pyruvate from cultured rat Sertoli cells. FSH and isoproterenol caused 3-6-fold stimulation of lactate and pyruvate secretion, whereas ovine LH, TSH, and prolactin were ineffective. Dibutyryl cyclic AMP (10(-4) M) stimulated the secretion of lactate and pyruvate to the same extent as FSH. Much lower stimulation was observed when Sertoli cells from 43-day old rats were exposed to FSH or isoproterenol. FSH increased lactate secretion in a concentration-dependent manner. The concentration of FSH (NIH-S14) causing half-maximal stimulation of lactate secretion (150 ng/ml) was similar to that causing 50% maximal stimulation of Sertoli cell adenylyl cyclase. Both FSH and isoproterenol caused a time-dependent increase in lactate levels in the incubation medium during the first 6-9 hr after the addition of hormones, after which levels were constant or decreased. Thus, the production of lactate and pyruvate by cultured Sertoli cells is stimulated both by FSH and isoproterenol and these effects are exerted via cyclic AMP.

Animals↗
PubMed1993

Diabetes prevents the normal responses of the ovary to FSH.

FSH in vitro stimulates increased oxygen uptake by isolated follicular granulosa cells from immature rats treated with diethylstilbestrol (DES) when substrates are present (glucose, glutamate, pyruvate or fumerate) or are completely absent. However, when glucose is the only substrate or when any single substrate is omitted from the buffer, FSH has no effect. FSH in vitro also increases the uptake of glucose and the formation of 14CO2 from [1-6 14C]-glucose. Granulosa cells from diabetic immature rats treated with DES did not show increased oxygen uptake with in vitro FSH. Diabetic cells had similar receptor binding of FSH to that of control non-diabetic cells. The addition of both insulin and FSH in vitro to buffer with diabetic granulosa cells gave increased oxygen uptake over that of control cells from diabetic rats. The insulin stimulation of oxygen uptake by FSH in cells from diabetic rats was not duplicated by either epidermal growth factor (EGF) or insulin-like growth factor I (IGF-1). Follicle counts of ovaries from diabetic and control immature rats treated with DES showed increased atresia in the diabetic ovaries after only 44 hr. of diabetes. Follicle counts of ovaries from adult diabetic rats showed increased atresia in 24 hours after induction of diabetes at proestrus. Follicle counts of pseudopregnant rats showed increased atresia by 3 days after diabetes was induced. We conclude that diabetes prevents normal follicle growth stimulated either by exogenous DES or by endogenous hormones secreted during proestrus.

Animals↗
PubMed2000

Effects of leptin on basal and FSH stimulated steroidogenesis in human granulosa luteal cells.

BACKGROUND: Body weight influences fertility and studies in mice have indicated that leptin is one of the mediators of this effect. Leptin is believed to centrally stimulate the hypothalamic-pituitary axis resulting in increased gonadotropin release. Moreover, leptin is present in follicular fluid and the receptor is expressed in the human ovary. The aim of this study was to evaluate the direct effect of leptin on cultured human granulosa cell steroidogenesis. METHODS: Granulosa cells were obtained in connection with IVF procedures, and then cultured in a serum-free medium containing androstenedione (1 microM) for a total of 4 days. After 2 days of culture the medium was changed and the hormones under study were added. We tested the effect of leptin (1, 20, 100 ng/ml) on basal, FSH (10-100 ng/ml), and FSH (10-100 ng/ml)+IGF-I (30 ng/ml) stimulated steroidogenesis. RESULTS: Leptin (20 ng/ml and 100 ng/ml) significantly reduced basal and FSH-stimulated estradiol secretion (p<0.05). Basal and FSH (10 and 30 ng/ml) stimulated progesterone production was significantly inhibited by leptin 20 ng/ml, whereas leptin 100 ng/ml significantly reduced basal but not FSH stimulated progesterone production. Finally, steroidogenesis stimulated by IGF-I alone and in combination with FSH was not influenced by leptin. CONCLUSION: These results suggest that leptin acts directly to inhibit basal and FSH stimulated estradiol and progesterone production in cultured human granulosa cells. This raises the possibility that high circulating leptin levels as seen in obese women may compromise fertility through peripheral mechanisms.

Body Weight↗
PubMed2000

FSH beta-subunit gene expression in long-term ovariectomized rat after pulsatile intracerebroventricular microinjections of GnRH.

OBJECTIVES: The purpose of this study was to examine whether in long-term ovariectomized rats direct pulsatile intracerebroventricular microinfusions of GnRH would result in frequency dependent biosynthesis of pituitary FSH beta-subunit mRNA. METHODS: Stainless steel cannula was stereotaxically implanted into the third ventricle of ovariectomized rats. 1 nM of GnRH microinjections were given at frequency 1, 2, 4 pulses/hour during 5 hours. Pituitary FSH beta-subunit mRNA level was determined by Northern-blot and serum FSH concentration was examined by RIA. RESULTS: Exogenous GnRH (1nM) induced a significant increase of pituitary content of FSH beta-subunit mRNA when administered 30 or 60 min intervals over 5 hours to ovariectomized rats. RESULTS: GnRH microinjections given at frequency of 1 pulse/hour were mostly effective resulting both in 85% increase of FSH beta-subunit mRNA level as compared to control as well as a significant (78%) stimulation of FSH release. CONCLUSIONS: our data show that in a long term ovariectomized rats (without steroid and gonadal peptides supplementation) a direct pulsatile intracerebroventricular microinjections of GnRH induce frequency-dependent pituitary FSH beta-subunit mRNA biosynthesis in the same mode as it was reported for gonadectomized and steroid replaced rats. It seems therefore that this method would represent an interesting alternative to the use of classical agents to disconnect, in vivo, the pituitary from hypothalamic GnRH influence. It may also provide a physiological data concerning regulatory aspects of gonadotropin subunits biosynthesis.

Journal Article↗
PubMed2002

Hypothalamic, pituitary and gonadal regulation of FSH.

FSH is a key reproductive hormone involved in the control of ovarian folliculogenesis and steroidogenesis. Multiple regulatory mechanisms govern the release of FSH. These regulatory mechanisms appear to work in concert to modulate the level, pattern and biological potency of circulating FSH, thereby adjusting the gonadotrophic stimulus to meet the challenge of a changing physiological need. This review (i) summarizes various neuroendocrine, autocrine and paracrine mechanisms involved in the control of FSH production and secretion; (ii) identifies possible mechanisms by which LH and FSH are differentially released from the same gonadotrophs; (iii) considers the means by which changes in the quality of the FSH signal are regulated and the implication of such changes; and (iv) emphasizes how large animal models have helped to advance our understanding of FSH control.

Animals↗
PubMed2003

Role of FSH and epidermal growth factor (EGF) in the initiation of steroidogenesis in granulosa cells associated with follicular selection in chicken ovaries.

In chicken ovaries, one small yellow follicle (SYF) is selected daily from a pool of follicles of similar size and becomes a preovulatory follicle. FSH induces follicular growth and steroidogenesis. Epidermal growth factor (EGF), an intraovarian hormone, suppresses granulosa cell differentiation. This study demonstrates that recruitment of SYFs into the hierarchy of preovulatory follicles is associated with a change in steroidogenic activity in granulosa cells regulated, at least in part, by FSH and EGF. Abundance of P450 side-chain cleavage (P450scc) mRNA was higher in the smallest preovulatory follicle (F6) compared with SYF, whereas FSH and EGF receptor (FSHr and EGFr, respectively) mRNA abundance was similar. FSH increased P450scc mRNA abundance and progesterone secretion and decreased FSHr mRNA in cultured granulosa cells, whereas EGF attenuated or suppressed P450scc mRNA and decreased FSHr mRNA abundance. None of the hormones influenced EGFr mRNA abundance. When used in combination, EGF attenuated or suppressed the stimulatory effect of FSH on the expression of P450scc mRNA and production of progesterone in a dose-dependent manner. The results indicate that (1) selection is associated with an increase in P450scc mRNA; (2) FSH stimulates expression of P450scc mRNA and progesterone secretion in granulosa cells of SYF; and (3) induction of P450scc mRNA and progesterone secretion by FSH is attenuated or blocked by EGF.

Animals↗
PubMed1976

[Investigations on LH and FSH serum levels before and after application of synthetic LH-releasing-hormone in healthy men of different age].

50 male healthy volunteers of different age had measurements of plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Basal levels of LH and FSH as well as maximal release of both hormones after i.v. application of 25 mug of synthetical LH-releasing hormone have been done. Results demonstrate an increasing reserve capacity of LH and FSH with age. FSH/LH ratio is altered in favor of FSH with duration of life. Sensitivity of gonadotropin producing cells of adenohypophysis to LH-releasing hormone is diminished in old age that can be recognized from a diminution of the relative rise of serum LH and FSH after LH-RH application. Correlations and partial correlations of absolute and relative body weight with age and basal LH and FSH serum levels demonstrate that age and not body weight plays a main part for increasing gonadotropin serum values. Causative responsibility for the increased LH serum concentrations is a decrease of testosterone production with age. Data obtained in this study and reports presented in literature give no convincing explanation for the increase of FSH serum levels with age.

Adolescent↗
PubMed1977

[Evidence of an epididymis factor inhibiting the hypothalamic synthesis of FSH-RH in the rat].

We have measured, by radioimmunoassay, FSH and LH in the blood plasma and in the hypophysis of castrated male rats, injected with epididymal inhibin; we have also evaluated the FSH and LH releasing activities of their hypothalamus by measuring plasma FSH and LH levels of spayed female rats, treated by hypothalamic extracts of the previous rats. The FSH and LH pituitary levels do not change compared with controls, and it is impossible to know if inhibin acts directly on hypophysis; it is likely that, directly or indirectly, inhibin restrains at the same time the synthesis and the release of FSH. On the contrary, the hypothalamic extracts lose their FSH-RH, but not their LH-RH, activities; then, inhibin operates on hypothalamus by suppressing of the synthesis of FSH-RH.

Animals↗