Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FSH”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,153 records · Page 64Linked to original sources
PubMedDate not supplied

Exploration of the testis in infertile men. Relationships among serum levels of FSH, LH, 17-alpha-OH-progesterone and testosterone.

A considerable body of evidence is available indicating a paracrine relationship between the seminiferous tubules and the Leydig cells. In 113 adult subjects in basal conditions the blood levels were determined of FSH (follicle stimulating hormone), LH (luteinizing hormone), 17-alpha-OH-P (17-alpha-OH-progesterone) and T (testosterone) either as a whole or as a free fraction. According to the sperm counts and the FSH levels, the studied subjects were divided into three groups: a group N (Normozoospermia) with sperm counts greater than 20 million/ml and FSH levels of 2.5 +/- 1.5 (mean +/- SD, mIU/ml), a group MO (moderate oligozoospermia) with mild degree of oligozoospermia (5-10 mill) and FSH levels in the range found in group N, a group SO (severe oligozoospermia) with severe degree of oligozoospermia (sperm count less than 5 mill/ml) and FSH levels greater than 2 SD the mean value in the N. Serum levels of LH, 17-alpha-OHP, total T, free T and FSH/LH, LH/T, 17-alpha-OHP/T ratios in group MO and SO were compared with those found in the group N.(ABSTRACT TRUNCATED AT 250 WORDS)

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

The influence of LH and/or FSH on Leydig and Sertoli cell morphology after testicular involution in the Djungarian hamster, Phodopus sungorus, induced by hypophysectomy or short photoperiods.

In the Djungarian hamster, Phodopus sungorus, the morphological alterations of Sertoli and Leydig cells were investigated under the influence of gonadotropins (LH and/or FSH) after testicular regression induced either by hypophysectomy or photoinhibition. Stimulation with LH or LH/FSH lead to a redifferentiation of morphological features of Leydig cells such as nuclear structure, smooth endoplasmic reticulum and size of cell and nucleus area within 7 days of hormone treatment. Similarly, stimulation with FSH or LH/FSH caused redifferentiation of Sertoli cell nuclear structure, rough endoplasmic reticulum and nuclear size within 7 days. Incomplete restoration of Leydig and Sertoli cell morphology was observed under FSH and LH treatment respectively. In both Leydig and Sertoli cells combined LH and FSH application resulted in an increased response in respect to morphological redifferentiation, possibly indicating paracrine regulatory mechanisms. In all groups treated an intact blood-testis barrier (BTB) was reestablished after a minimum of 7 days, indicating that the existence of the blood-testis barrier is not dependent on specific gonadotropin supply but on the developmental stage of the seminiferous epithelium. Sham-operated animals showed increased cell and nucleus area of Leydig cells in comparison to photostimulated animals. After testicular involution as well as after LH or FSH treatment there were no significant morphological differences between hypophysectomized and photoinhibited animals in respect to the documented ultrastructural and morphometrical characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Inhibin and steroid response to testicular stimulation with pure FSH (Metrodin) in infertile men with unilateral cryptorchidism.

Static measurements of immunoreactive inhibin have proven of little relevance in the diagnosis of testicular disorders. Dynamic evaluation of the inhibin secretory reserve might detect a specific Sertoli cell defect in a subgroup of infertile men. We compared the response of inhibin and steroids to an intravenous injection of pure FSH (Metrodin, Serono, 300 IU) in 13 infertile men with unilateral cryptorchidism to that in eight normal fertile men. Blood was aspirated before, 24, 48, and 72 h after the FSH injection. Two subgroups of patients with unilateral cryptorchidism were detected: those who responded by secreting inhibin in a pattern similar to normal men (seven patients), and those who responded poorly or not at all (six patients). The presumed cause of this difference is a defect of Sertoli cell reserve function due to a combination of insults to the testes, and not to cryptorchidism itself. The difference in response to FSH cannot be predicted from semen analysis nor from static hormone measurements. Overall, inhibin levels correlated significantly with the serum concentrations of FSH (r = -0.36, P < 0.05), testosterone (r = 0.37, P < 0.05), and 17-hydroxyprogesterone (r = 0.66, P < 0.001). It is concluded that, in infertile men with unilateral cryptorchidism, Stimulation of Sertoli cells by FSH can identify a subgroup of patients with Sertoli cell malfunction involving inhibin synthesis.

Adult↗
PubMed2005

Oestradiol and FSH in gestational trophoblastic disease: a prospective analysis of their predictive value.

OBJECTIVE: To determine whether oestradiol or follicle-stimulating hormone (FSH) measured prior to treatment could improve the predictive value of the risk score used to determine treatment in cases of persistent gestational trophoblastic disease (GTD). DESIGN: Prospective observational study. SETTING: Tertiary referral centre for GTD. POPULATION: All women referred to Weston Park Hospital, Sheffield, with GTD between 1st January 1996 and 31st December 2000. METHODS: Blood was taken prior to the initiation of treatment to measure oestradiol and FSH. The results were analysed with respect to the time taken for the beta-hCG to return to normal. MAIN OUTCOME MEASURES: Time taken to reach a normal beta-hCG. RESULTS: Data on 118 women were collected. Three women died of GTD during follow up. Using Cox's proportional hazards regression analysis, division of the risk scores into high and low risk groups (</=7, >7) demonstrated a significant difference with regard to the length of time taken to reach a normal beta-hCG level (hazard ratio 0.32; 95% CI: 0.18, 0.57) comparing high risk relative to low risk. However, addition of neither oestradiol nor FSH to the Cox regression analysis produced a significant hazard ratio (Ln oestradiol, 0.95; FSH 0.99). Division of the patients' risk scores into three groups of low (0-4), intermediate (5-7) and high (>7) risk groups produced similar results. CONCLUSIONS: The measurement of neither oestradiol nor FSH appears to improve the prediction of outcome in persistent GTD when added to the risk score.

Adult↗
PubMed1995

Comparative studies on the effects of specific immunoneutralization of endogenous FSH or LH on testicular germ cell transformations in the adult bonnet monkey (Macaca radiata).

PROBLEM: It is yet to be determined clearly whether the two hormones FSH and T act synergistically in the same cell type--the Sertoli cells--to control overall spermatogenesis or influence independently the transformation of specific germ cell types during spermatogenesis in the adult mammal. METHOD: Adult male bonnet monkeys specifically deprived of either FSH or LH using immunoneutralization techniques were monitored for changes in testicular germ cell transformation by DNA flow cytometry. RESULTS: FSH deprivation caused a significant reduction ( > 40%; P < 0.05) in [3H] thymidine incorporation into DNA of proliferating 2C (spermatogonial) cells, a marked inhibition ( > 50%) in the transformation of 2C to primary spermatocytes (4C) and a concomitant, belated reduction (50%) in the formation of round spermatids (1C). In contrast, specific LH/T deprivation led to an immediate arrest in the meiotic transformation of 4C to 1C/HC leading to an effective and significant block ( < 90%; P < 0.01) in sperm production. CONCLUSION: Thus, LH rather than FSH deprivation has a more pronounced and immediate effect as the former primarily blocks meiosis (4C --> 1C/HC) which controls production of spermatids. These data provide evidence for LH/T and FSH regulating spermatogenic process in the adult primate by primarily acting at specific germ cell transformation steps.

Animals↗
PubMed1980

The significance of FSH elevation in young women with disorders of ovulation.

High serum follicle stimulating hormone (FSH) values are consistent with ovarian failure. We studied the progress of 67 women aged under 35 years with oligomenorrhoea or secondary amenorrhoea in whom the serum FSH value was greater than 20 U/1. Twenty-four patients remained amenorrhoeic, but 17 ovulated and six conceived, two on two occasions. Coincident mean serum luteinising hormone (LH) concentrations were significantly lower and mean total urinary oestrogen concentrations were significantly higher in patients who subsequently ovulated, but the degree of increase in FSH did not correlate well with later ovarian function. Treatment with oestrogens, clomiphene citrate, human pituitary gonadotrophin, and bromocriptine was of no benefit in inducing an ovarian response while FSH concentrations remained raised. Our results suggest that a considerable proportion of younger women with ovulatory disorders associated with FSH values in the menopausal range will spontaneously resume ovulation and some will conceive.

Adult↗
PubMed1985

Somatomedin C augments FSH-induced differentiation of cultured rat granulosa cells.

Growth hormone (GH) deficiency in rats is associated with decreased ovarian steroidal responsiveness to gonadotropins, possibly through a reduction in the production of the GH-dependent Somatomedin C/insulinlike growth factor I (SM C/IGF I). We have investigated the direct effects of synthetic SM C/IGF I on gonadotropin-stimulated ovarian steroidogenesis in vitro. Granulosa cells were cultured in a serum-free medium for 48 h in the presence of follicle-stimulating hormone (FSH), with or without SM C/IGF I. FSH dose-dependently increased both estrogen and progestin production. Concomitant treatment with SM C/IGF I led to a dose-dependent augmentation of progestin secretion over the full range of FSH doses tested, by a maximum of 2.3- to 2.6-fold. FSH-stimulated estrogen was enhanced by up to 2.4-fold but only at low doses of FSH. SM C/IGF I-enhanced progestin production was associated with increased pregnenolone production and 3 beta-hydroxysteroid dehydrogenase activity, whereas augmented estrogen production appeared to be due to enhanced aromatase activity. The actions of SM C/IGF I, at physiologically relevant concentrations were correlated with increased extracellular cAMP accumulation and cellular protein content but were independent of any change in cell number or viability. In contrast to SM C/IGF I, the closely related peptide multiplication-stimulating activity decreased estrogen production while increasing progestin metabolite accumulation. The present results indicate that the GH-dependent peptide SM C/IGF I may play a role in ovarian development by enhancing gonadotropin-stimulated granulosa cell steroidogenesis.

20-Hydroxysteroid Dehydrogenases↗
PubMed1985

Decreased in vitro secretion of LH, FSH, and free alpha-subunits by pituitary cells from old male rats.

Various in vivo and in vitro pituitary-Leydig cell functions were examined in mature (5-8 mo) vs. old (22-25 mo) male Wistar rats. Old rats exhibited decreased serum concentrations of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) (P less than 0.0025) but similar levels of prolactin (P less than 0.01) both before and 4 wk after castration. The in vitro release of LH, FSH, and free alpha-subunits was measured in primary cultures of dispersed anterior pituitary cells from both intact and castrated rats. During 48 h of incubation, basal secretion rates of the glycoproteins were decreased (P less than 0.001) from cells of both intact and castrated old rats. After stimulation with LH-releasing hormone (LRH) in single (10(-8) M) or multiple (10(-10) - 10(-7) M) doses, the total amounts of the glycoproteins secreted were also less from cells of both intact and castrated old rats. However, repeated measures analysis of variance revealed age-related hyporesponsivity to LRH stimulation only for LH secretion by cells from intact rats. The basal molar ratios of alpha/(LH + FSH) secreted by cells from intact but not castrated old rats were lower than those from cells of the corresponding mature rats. Moreover, after LRH stimulation (10(-10) - 10(-7) M), molar secretory ratios of alpha/(LH + FSH) decreased from cells of intact mature rats but increased from cells of intact old rats. These in vitro data suggest that the reduced serum LH and FSH levels in intact and castrated old male rats result in part from decreased secretion of these glycoproteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1984

Differential suppression of FSH and LH secretion by follicular fluid in the presence or absence of GnRH.

The differential role of porcine follicular fluid (pFF) in regulating follicle-stimulating hormone (FSH) and luteinizing hormone (LH) release in vivo in situations of different gonadotropin releasing hormone (GnRH) backgrounds was studied. In experiment 1, 2-week ovariectomized rats injected intravenously with 4, 16 or 64 mg of protein from pFF, showed a dose-dependent suppression of FSH over time, with a maximal suppression to 40% of control values by 10 h. LH levels were slightly, but significantly, elevated by the two lower doses, but not by the highest dose of pFF. In experiment 2, 64 mg pFF was superimposed (i.v. injection) in ovariectomized rats injected subcutaneously with a high dose of GnRH antagonist (500 micrograms) 24 h earlier. The pFF suppressed FSH 35% below the level achieved in the absence of GnRH stimulation, with no effect on LH. In experiment 3, the rise in FSH secretion in acutely ovariectomized rats was shown to be inhibited by 8 or 32 mg pFF administered intravenously 3.5 h after surgery. Injection of GnRH (250 or 1,000 ng) 4.5 h after pFF could not overcome the inhibitory action of pFF on FSH, although non-pFF-treated controls responded in a dose-dependent fashion to GnRH stimulation. The expected LH response to GnRH was not affected by pFF, except in the group receiving 1,000 ng GnRH and 8 mg pFF. In these rats, LH was enhanced in one trial, but suppressed in a replicate trial, illustrating the inconsistent effects of pFF on LH under conditions of high GnRH stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Endogenous excitatory amino acid regulation of the progesterone-induced LH and FSH surge in estrogen-primed ovariectomized rats.

The role of endogenous excitatory amino acid neurotransmission in the regulation of progesterone and triamcinolone acetonide-induced LH and FSH release was examined. Estrogen-primed ovariectomized rats were utilized in this study. Progesterone or triamcinolone acetonide (1 mg/kg body weight) treatment led to a highly significant elevation of serum LH and FSH levels 5 h later. Treatment with the selective noncompetitive NMDA receptor antagonist, MK801, had no effect on serum LH and FSH levels when compared to estrogen controls. However, MK801 administered 1 h prior to progesterone or triamcinolone acetonide administration completely blocked their ability to induce LH and FSH surges. These studies demonstrate for the first time the involvement of endogenous excitatory amino acid neurotransmission in the mediation of progesterone and corticosteroid-induced LH and FSH surges.

Animals↗
PubMed1985

Effects of the intraventricular administration of 5,7-dihydroxytryptamine on FSH, LH and prolactin secretion in neonatally estrogenized male rats.

The role of the serotoninergic system in the control of LH, FSH and prolactin secretion was analyzed in control and neonatally estrogenized male rats. Animals injected s.c. with 500 micrograms of estradiol benzoate (EB) on day 1 of life, or their corresponding sham-treated controls, were divided on day 75 into the following groups: (1) orchidectomized; (2) injected intraventricularly with 5,7-dihydroxytryptamine (5,7-DHT); (3) orchidectomized and treated with 5,7-DHT, and (4) sham operated. 15 days later, the animals were decapitated and their FHS, LH and prolactin plasma values measured by specific RIA systems. After the treatment with 5,7-DHT, control animals showed a decline in basal prolactin levels but no modification in basal LH and FSH values. After castration, 5,7-DHT-treated animals showed a reduced LH increase and a more marked prolactin decrease. In neonatal estrogen-treated animals, the 5,7-DHT injection did not change FSH, LH or prolactin levels but did partially or completely abolish the post-castration rise in FSH and LH levels, respectively. These data seem to indicate that neonatal estrogenization induced a modification of the serotoninergic role in the control of LH, FSH and prolactin.

Animals↗
PubMed1978

Inhibition of de novo synthesis of FSH by the Sertoli cell factor (SCF).

The effects of SCF, a substance produced by isolated rat Sertoli cells in culture, on the synthesis of FSH and LH were studied in vitro. Anterior pituitaries from adult male rats were organ-cultured 24-48h in the presence and absence of SCF in the culture medium. The incorporation of 3H-leucine into FSH and LH was determined following 6h incubation with this labelled precursor and immunoprecipitation with specific FSH or LH antibodies. Total FSH and LH were measured by radioimmunoassay. The results indicate that SCF can selectively reduce the incorporation of 3H-leucine into immunoprecipitable FSH without decreasing the incorporation into LH.

Animals↗
PubMed1983

Regulation of cytochrome P-450scc in immature porcine granulosa cells by FSH and estradiol.

FSH, estradiol, or a combination of FSH and estradiol enhanced secretion of progesterone by primary cultures of immature porcine granulosa cells; they also increased the mitochondrial content of cytochrome P-450 and mitochondrial cholesterol side-chain cleavage activity. FSH or estradiol alone increased mitochondrial cytochrome P-450 levels and cholesterol side-chain cleavage activity to a similar extent. The combination of FSH and estradiol further increased cytochrome P-450 and side-chain cleavage activity. Our results demonstrate that FSH, estrogen and the combination of the hormones stimulate progestin synthesis by granulosa cells, at least in part, by increasing cholesterol side-chain cleavage enzyme levels. These observations suggest a dual hormonal regulation of the enzyme catalyzing the rate-limiting step in the biosynthetic pathway of steroid hormones.

Animals↗
PubMed1991

Cortisol in vivo increases FSH beta mRNA selectively in pituitaries of male rats.

Cortisol treatment for 6 or 12 days had no effect on serum FSH in intact males and animals castrated for 1 or 7 days, but pituitary FSH was increased by the steroid in both intact and castrate groups. In contrast, cortisol inhibited serum LH in both intact and castrated animals while only increasing pituitary levels of LH in 7 day castrates. Cortisol also increased the mRNA for FSH beta without affecting alpha or LH beta mRNAs. These data suggest that the selective increase in pituitary content of FSH may be due to a selective increase in FSH beta mRNA following exposure to cortisol.

Animals↗
PubMed1975

Patterns of LH and FSH release from perifused rat pituitaries in response to infusions of hypothalamic extract.

A continuous flow incubation (perufusion) system was developed in which the secretory responses of pools of hemipituitaries from adult male rats to hypothalamic extract (HE) were characterized by serial radioimmunoassay of LH and FSH in the effluent medium. There was in initial massive release of LH and FSH which, in the absence of HE, declined to low basal levels at a rate which depended on the flow rate. Thereafter, the baseline for LH continued to decline gradually while that for FSH was stable. The rate of LH and FSH release rose abruptly after addition of the HE to the medium and returned promptly to baseline after withdrawal of the HE. During continuous infusion of HE for five hours, LH secretion was maintained at a relatively constant, elevated level. The responses to repeated identical pulses of HE were highly reproducible. The variability between responses by any one pool of tissue was significantly less than between responses of separate pituitary pools including pools comprising right and left halves of the same glands. For any given pool of pituitaries of the relationships were linear between: 1) duration of HE pulses (concentration constant) and increases in LH output, and 2) log of concentration of HE (pulse duration constant) and increases inLH and in FSH output. Consistent responses were obtained for up to 12 hr, the maximum period tested.

Animals↗
PubMed1975

Direct effect of testosterone and its 5alpha-reduced metabolites on pituitary LH and FSH release in vitro: change in pituitary responsiveness to hypothalamic extract.

A continuous flow incubation (perifusion) system was used to examine the effect of testosterone (T) and three of its 5alpha-reduced metabolites, dihydrotestosterone (DHT), 5alpha-androstane-3alpha, 17beta-diol (3alpha-Adiol) and its 3beta-epimer (3beta-Adiol) on LH and FSH release, induced by hypothalamic extract (HE). In the absence of steroids, successive identical pulses of HE, of 10 min duration each, administered at hourly intervals over a 8-hr period, caused highly reproducible release of LH and FSH. In experimental perifusions, the amounts of LH and FSH released in response to standard 10-min pulses of HE administered at hourly intervals during the continuous infusion of steroid for 4-6 hr were compared with the responses of the same pituitaries to the standard test pulses of HE given before the start of the steroid infusion and after its cessation. All the androgens tested altered pituitary responsiveness. At the 0.1 and 1.0 mug/ml dose level there were differences between the steroids in the way they influenced the responsiveness of the pituitary overtime. Their effects at these two doses fell into three categories depending on whether there was initially: 1) an augmentation of HE induced LH release (T and 3beta-Adiol), 2) augmentation of both FSH and LH release (DHT), OR 3) NO AUGMENTATION IN THE RELEASE OF EITHer gonadotrophin (3alpha-Adiol). All the androgens ultimately suppressed pituitary responsiveness to HE and all were associated with changes in the ratios of LH and FSH released. When the dose of T and 3 beta-Adiol was raised to 10 mug/ml or that of DHT lowered to 0.01 mug/ml the initial stimulatory phase was not seen. Epitestosterone, the biologically inactive epimer of T, did not alter the responsiveness of the pituitary of HE.

Androstanes↗
PubMed1975

Partial masculinization of rat liver enzyme activities following treatment with FSH.

The metabolism of 4-(4014C)androstene-3,17-dione and 5alpha-(4-14C)androstene-3alpha, 17beta-diol was studies in the microsomal fraction and that of 4-(4-14C) androstene-3,17-dione in the 105,000 times g supernatant fraction of livers from castrated male and female rats treated with LH and FSH. Administration of LH led to significant decreases in 17-hydroxysteroid reduction and 7alpha-hydroxylation of 4-androstene-3,17-dione in both male and female rats and in 6beta-hydroxylation of 4-androstene-3,17-dione in female rats. FSH on the other hand specifically stimulated (masculinized) the following sex-dependent hydroxylations: 16alpha-hydroxylation of 4-androstene-3,17-dione in female rats and 2alpha-, and 2beta- and 18-hydroxylation of 5alpha-androstane-3alpha,17beta-diol in male rats. The metabolism of 4-androstene-3,17-dione and 5alpha-androstane-3alpha,17beta-diol was also studied in castrated male and female rats given testosterone propionate and in castrated female rats given testosterone propionate in combination with LH or FSH. It was shown that neither LH nor FSH could compensate for the relative androgen-unresponsiveness exhibited by female as compared to male rats. It is concluded that FSH but not LH may participate in the regulation of sex-dependent hydroxylase systems in rat liver.?2,Author

17-Hydroxycorticosteroids↗
PubMed1975

An in vivo assay for anti-LH-RH and anti-FSH-RH activity of inhibitory analogues of LH-RH.

A convenient and sensitive method for testing anti-LH- and FSH-releasing activities of antagonists of LH-RH was devised. The peptides to be tested were injected subcutaneously together with synthetic LH-releasing hormone (LH-RH) in immature male rats. Serum LH and FSH concentrations were measured 30 min later by radioimmunoassay. In this system, [DesHis2]-LH-RH failed to block the pituitary response to LH-RH in agreement with previous data. The administration of [DesHis2, desGly10]-LH-RH ethylamide, [Des-His2, Leu3, des Gly10]-LH-RH ethylamide, [Des-His2, D-Ala6, des-Gly10]-LH-RH ethylamide, and [DESHis2, D-Ala6]-LH-RH in doses of 200 mug/rat, and [DesHis2, Leu3, D-Ala, desGly10]-LH-RH ethylamide in doses ranging from 100-400 mug/rat caused a significant inhibition of LH-RH-induced release of LH and FSH. On the other hand, [DesHis2, desGly10]-LH-RH propylamide, and [Leu2, Leu3, D-Ala6, desGly10]-LH-RH ethylamide failed to block the response to LH-RH. Among the peptides tested, [DesHis2, d-ala6, desGly10]-LH-RH etylamide, [Leu2, Leu3, D-Ala, desGly10]-LH-RH ethylamide in doses of 200 mug and [DesHis2, Leu3, D-Ala6, desGly10]-LH-RH ethylamide in a dose of 400 mug/rat showed some intrinsic LH and FSH-releasing activities. The method described here is simple and convenient for studying the anti-LH-RH release activity of inhibitory analogues of LH-RH, and also enabled us to demonstrate for the first time an in vivo inhibition of FSH release by these analogues.

Animals↗