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PubMed1998

Hypokalemia alters sex hormone and gonadotropin levels: evidence that FSH may be required for luteinization.

Hypokalemia produced different effects on steroid sex hormone concentrations in plasma and ovary in the mouse. Estradiol levels were slightly increased, whereas circulating progesterone was markedly decreased in all estrous periods. The preovulatory surge of gonadotropins and the secondary surge of follicle-stimulating hormone (FSH) at estrus were also decreased, but basal levels of both gonadotropins were unaffected. Supplementation with luteinizing hormone (LH), FSH, or gonadotropin-releasing hormone (GnRH) at proestrus rapidly normalized plasma and ovarian progesterone levels at this stage of the estrous cycle. Plasma progesterone levels at diestrus were restored only by combined treatment, at the periovulatory stage, with LH and FSH or GnRH but not by LH or FSH alone. The results demonstrate a lack of steroidogenic activity in the corpus luteum of the potassium-deficient mice and, furthermore, that FSH plays an important role in luteinization in the hypokalemic mice. We conclude that alteration of the transcellular potassium gradient may affect the regulation of the periovulatory surge of gonadotropins and progesterone secretion, probably by altering the release of GnRH from the hypothalamus. In addition, the results suggest that FSH may play a certain role as a luteotropic hormone in mice.

Animals↗
PubMed2001

Identification of genomic regions controlling plasma FSH concentrations in Meishan-White Composite boars.

The Chinese Meishan (ME) breed of pig is unique for many reproductive traits. Compared with Western breeds of swine, ME females reach puberty earlier, ovulate more ova per estrus, and have greater uterine capacity, while intact males (boars) have smaller testes and extremely elevated plasma levels of pituitary-derived glycoprotein hormones. In an effort to identify the genetic mechanisms controlling the elevated plasma levels of pituitary-derived glycoprotein hormones [in particular, follicle-stimulating hormone (FSH)] and to determine whether some of these genetic factors are also responsible for differences in other phenotypes, we scanned the entire genome for regions that affected plasma FSH in boars from a Meishan-White Composite (equal contributions of Chester White, Landrace, Large White, and Yorkshire) resource population. Initially, the entire genome of 121 boars was scanned for regions that potentially influenced plasma FSH. The most significant genomic regions were further studied in a total of 436 boars. Three genomic regions located on chromosomes 3, 10, and X apparently possess genes that significantly affect FSH level, and one region provided suggestive evidence for the presence of FSH-controlling genes located on chromosome 8. The region on the X chromosome also affected testes size. Similar genomic regions to those identified on chromosomes 3, 8, and 10 in this study have been identified to affect ovulation rate in female litter mates, supporting the hypothesis that plasma FSH in pubertal boars and ovulation rate in females is controlled by a similar set of genes.

Animals↗
PubMed1981

Evidence for a hypothalamic site of action of inhibin to suppress FSH release.

To determine if inhibin has a hypothalamic site of action to suppress FSH release, highly purified inhibin preparations from the rete testis fluid (RTF) of rams were injected into adult male rats which had been orchidectomized (ORDX) 24 hours earlier. Third ventricular (3rd V) injection of a potent inhibin fraction (RTF 38-I) significantly depressed plasma FSH concentrations, without influencing LH, 4-10 h after treatment. A less active preparation of inhibin (RTF 38-II) at the same dose had no effect. A higher dose of another less potent fraction (RTF 1A) significantly reduced FSH 2-6 h following 3rd V administration, accompanied by slight but significant decrements in LH at 2 and 4 only. To determine responsiveness of the pituitary, luteinizing hormone-releasing hormone (LHRH) was injected intravenously at 6 h. It induced similar elevations of FSH and LH in inhibin- and saline-treated groups. Systemic administration of RTF 38-II at a dose 2.5-fold higher than the dose effective centrally failed to modify either FSH or LH levels up to 6 h. These results provide evidence that inhibin from the male can preferentially suppress FSH release by a CNS site of action in addition to its well-known pituitary site of action.

Animals↗
PubMed1975

Hormonal influences on the level of testicular androgen binding activity: effect of FSH following hypophysectomy.

Concentrations of high affinity (Ka equals 5.5 plus or minus 0.83 times 10-8M-1) androgen binding activity in carbonextracted rat testicular supernatants have been determined by Scatchard plot analysis under a variety of hormonal situations: (a) 0-90 days following hypophysectomy; (b) 0-60 days of daily injection of NIH-FSH-P1 (150 mug) beginning 1 day after hypophysectomy; and (c) 0-60 days of daily FSH treatment beginning 30 days after hypophysectomy. The high affinity binding component declined from 0.32 pmoles/mg protein intact adults to 0.28, 0.17, and less than 0.08 (limit of detectability) pmoles/mg protein at 11, 16 and 31 days, respectively. FSH treatment beginning immediately after surgery slowed this decline, giving values of 0.30, 0.17, and 0.12 pmoles/mg protein after 11, 29, and 54 days of treatment, respectively. Expressed as pmoles per testis this represented 96, 61, and 40% of the intact control level. Similar effects on the level of androgen binding protein (Rf 0.54) were measured by steady-state polyacrylamide gel electrophoresis (PAGE). The concentration in both testis and epididymis declined gradually to nondetectable levels by 30 days after surgery. FSH treatment for 11, 29, and 54 days, respectively, resulted in 0.37, 0.38, and 0.03 pmoles of sites/mg protein in testis compared to 0.34 in intact controls and 5.7, 2.6, and 0.2 pmoles/mg protein in epididymis compared to 2.8 in intact controls. Doses of 80, 150, and 300 mug FSH/rat/day for 3 days beginning 30 days after hypophysectomy when postmeiotic elements of the germinal epithelium had degenerated caused graded increases in both testicular and epididymal levels of androgen binding protein. Prolonged FSH treatment (150 mug) under these conditions resulted in an increase in binding activity to a level of 0.12, 0.19, 0.17, and 0.20 pmoles/mg protein after 3, 11, 25, and 56 days of treatment. On a per testis basis this represented less than 20% of intact control levels. PAGE estimates were comparable except at the long treatment intervals. These results indicate that FSH treatment influences the level of androgen binding protein in adult testis and epididymis. This may reflect a direct influence on synthesis, degradation, and transport and/or indirect effects on general maintenance and responsiveness of the pertinent cell types.

Animals↗
PubMed1976

Selective effect of androgens on LH and FSH release in anterior pituitary cells in culture.

A possible direct effect of androgens at the pituitary level on gonadotropin release was studied using rat anterior pituitary cells in primary culture. The preincubation of cells with 3 X 10(-9)M testosterone (T) for 40 h increased the concentration of luteinizing hormone-releasing hormone (LHRH) required for half-maximal stimulation (ED50) of LH release from 3 X 10(-10)M to 1 X 10(-9)M. In the same experiment, the LHRH ED50 for FSH release (3 X 10(-10)M) was not affected by preincubation with T, while a slight stimulatory effect of the androgen was observed on balal FSH release and on the maximal FSH response to LHRH. Time-course experiments showed that the inhibitory effect of T on the LH response to LHRH was maximal after about 48 h of incubation and that 54 h after the removal of T, only 50% of the inhibition was reversed. 5 alpha-Dihydrotestosterone (DHT) and T led to the same maximal inhibition (15-20% of control) of the LH response to 10(-10)M LHRH. DHT was, however, about 3 times more potent than T, their ED50 values being 1.6 X 10(-10)M and 5 X 10(-10)M, respectively. In contrast to the effect on LH, the FSH response to 10(-10)M LHRH was only slightly, but not significantly, inhibited by increasing concentrations of DHT or T. The finding that total LH (medium + cell content) remained constant after incubation with T or DHT clearly indicates that the inhibition of the LH response to LHRH is really due to changes in the sensitivity of the releasing mechanisms in the LH-secreting cells. Androgens did, however, lead to increased total FSH. The present data indicate an independent control of LH and FSH secretion by a direct action of androgens at the pituitary level.

Androgens↗
PubMed1992

Passive immunoneutralization with a monoclonal antibody reveals a role for endogenous activin-B in mediating FSH hypersecretion during estrus and following ovariectomy of hypophysectomized, pituitary-grafted rats.

Recently, we reported that ovariectomy (OVX)-induced FSH hypersecretion can be elicited in hypophysectomized rats bearing renal pituitary allografts isolated from direct hypothalamic intervention. The possible role of the FSH-stimulating protein, activin-B, in eliciting this response was investigated using passive immunoneutralization with a monoclonal antibody (MAb) generated against activin-B. Other hypophysectomized/pituitary-grafted (H/G) rats serving as controls received an equivalent amount of a MAb incapable of neutralizing the biological actions of activin-B. Administration of increasing doses of the MAb prior to OVX dose-dependently suppressed serum FSH levels 12 h after OVX. Less consistent effects were observed 24 h after OVX even though an additional injection of the MAb was given 12 h after OVX in one study. Since it has been postulated that the periovulatory increase in additional injection of the MAb was given 12 h after OVX in one study. Since it has been postulated that the periovulatory increase in FSH secretion on estrus which is important for recruitment of follicles is a hypothalamic-independent phenomena, a separate experiment was performed in order to ascertain whether a local regulatory mechanism involving activin-B is operative on estrus. As in the preceding study using H/G rats, administration of the activin-B MAb on the evening of proestrus significantly attenuated serum FSH rises early on estrus. These results are consonant with the evolving concept that an important mechanism exists within the anterior pituitary proper for regulation of FSH secretion that involves the autocrine actions of activin-B.

Activins↗
PubMed2002

Paracrine regulation of FSH by follistatin in folliculostellate cell-enriched primate pituitary cell cultures.

Primary pituitary cell cultures are an important tool for understanding pituitary hormone gene expression. In the course of study of pituitary cell cultures from nonhuman adult male primates, pituitary secretory cells were noted to be rapidly overgrown by epithelioid cells with the morphological, immunocytochemical, and proliferative characteristics of folliculostellate cells. Using competitive RT-PCR assays, follistatin mRNA levels were found to increase 4-fold as folliculostellate cells proliferated with time in culture, whereas FSH-beta mRNA and FSH secretion were suppressed. Follistatin gene expression was stimulated by activin-A and pituitary adenylate cyclase-activating polypeptide but not by [D-Trp(6)]-GnRH ethylamide. Testosterone (T) also increased follistatin mRNA levels and follistatin protein secretion. FSH-beta mRNA was stimulated by [D-Trp(6)]-GnRH ethylamide and activin but was suppressed by T. The reciprocal relationship between follistatin and FSH-beta mRNA levels as folliculostellate cells proliferate with time in culture implies a role for folliculostellate cells in the follistatin-activin system in primates. The actions of GnRH and T on follistatin and FSH-beta mRNA levels in these cultures were opposite to effects observed in pituitary cultures from rats and identify species differences in the control of FSH production that may be folliculostellate cell-related.

Activins↗
PubMed2004

Testicular anti-mullerian hormone secretion is stimulated by recombinant human FSH in patients with congenital hypogonadotropic hypogonadism.

Serum anti-Mullerian hormone (AMH), a prepubertal Sertoli cell marker, declines during puberty as an early sign of testicular testosterone (T) production. When T synthesis or action is impaired, serum AMH is abnormally high in the first months after birth and at puberty but normal between these two periods. We postulated that FSH might be responsible for AMH up-regulation in the absence of androgen inhibition. To test this hypothesis, we administered recombinant human (rh) FSH to eight patients aged from 18-31 yr with untreated congenital hypogonadotropic hypogonadism. This situation is ideal to study the effect of FSH on AMH production because it avoids interference by endogenous gonadotropins and T. The patients received daily sc injections of 150 IU rhFSH for 1 month, followed in seven of them by a combined treatment of rhFSH plus human chorionic gonadotropin (hCG; 1500 UI im, twice a week) for 2 months. Gonadotropins, T, AMH, and inhibin B were measured in plasma before treatment every 10 d during rhFSH treatment and every month during combined rhFSH and hCG treatments. All hormones were at prepubertal levels before treatment. Although LH and T did not vary, AMH and inhibin B levels gradually increased after 20 d of FSH administration. However, in contrast to rhFSH alone, the combined rhFSH plus hCG stimulation of the testis dramatically suppresses the secretion of AMH and induced a modest but significant reduction of circulating inhibin B levels. We conclude that FSH stimulates AMH production in the testis when it is at a prepubertal stage. In addition, the decrease of serum AMH during combined rhFSH and hCG testicular stimulation is in agreement with the concept that during pubertal development and in adult life, the suppressive effect of LH-driven testicular androgens outweighs the stimulating effect of FSH on AMH production by Sertoli cells. Finally, the hCG-induced decrease in inhibin B suggests that in humans, as previously demonstrated in monkeys, testicular T is also able to inhibit inhibin B secretion.

Adolescent↗
PubMed1975

Serum LH and FSH responses to synthetic gonadotropin-releasing hormone in normal men.

The effects of dose and of age on the serum LH and FSH responses to synthetic gonadotropin-releasing hormone (GnRH) were determined in normal men. GnRH was given as in iv bolus in doses from 2 to 500 mug to each of nine normal men, 20-39 years old. The mean (+/- SE) maximum delta LH (maximum increment above the basal concentration) in response to each dose of GnRH was 2 mug, 7.2 +/- 1.7 mIU/ml; 10 mug, 15.7 +/- 3.4 mIU/ml; 50 mug, 37.7 +/- 9.6 mIU/ml; 250 mug, 47.8 +/- 11.2 mIU/ml; and 500 mug, 49.3 +/- 11.2 mIU/ml. The mean delta FSH in response to each dose was 2 mug, 0.5 +/- 0.2 mIU/ml; 10 mug, 0.8 +/- 0.2 mIU/ml; 50 mug, 1.2 +/- 0.3 mIU/ml; 250 mug, 2.0 +/- 0.3 mIU/ml; and 500 mug, 2.4 +/- 0.4 mIU/ml. Since both the LH and FSH responses to the 250 mug dose were significantly greater than those to smaller doses, but the responses to the 500 mug dose were not still larger, 250 mug was used as the standard test done for subsequent studies. The effect of age was tested by administering a 250 mug dose of GnRH as an iv bolus to 42 carefully selected normal men, 14 in each of three age groups, 20-39, 40-59, and 60-79 years old. Dialyzable serum testosterone levels decreased with increasing age, from 21.7 +/- 4.6 to 16.0 +/- 4.9 to 14.3 +/- 3.8 ng/dl (mean +/- SD), and the basal serum LH levels increased slightly, from 7.4 +/- 3.4 to 9.6 +/- 3.1 to 10.8 +/- 3.2 mIU/ml, suggesting that a slight degree of primary Leydig cell failure occurs with increasing age. There was no corresponding increase in mean maximum delta LH in response to GnRH with increasing age, despite the elevation in mean basal LH levels. The maximum delta LH/basal LH ratio, in fact, declined from 6.8 to 5.1 to 3.3 in the three age groups. The basal serum FSH levels did not change with increasing age, but the mean delta FSH values decreased from 3.0 +/- 0.5 to 2.9 +/- 1.1 +/- 0.3 mIU/ml. These data demonstrate decreased LH and FSH responses to synthetic GnRH, as well as some primary Leydig cell failure, in the male senescence.

Adult↗
PubMed1988

Evidence of differential control of FSH and LH secretion by gonadotropin-releasing hormone (GnRH) from the use of a GnRH antagonist.

The differential regulation of immunoactive FSH and LH secretion by endogenous GnRH was studied using a GnRH antagonist, [Ac-D2Nal1,D4FPhe2,DTrp3,DArg6]GnRH (the NAL-ARG antagonist), in normal women in the early follicular phase of the menstrual cycle, and their responses were compared to those in two groups of control women. Pulsatile LH secretion was examined as an index of the completeness of blockade of endogenous GnRH secretion. There was a dose-dependent decrease in both the frequency and amplitude of LH pulses. At the highest dose, LH pulses were completely abolished within 20 min after sc administration of the GnRH antagonist and for a minimum of 8 h in all women. The mean plasma LH levels were reduced within the first 4 h after antagonist administration at all doses (P less than 0.001). The duration of LH suppression was influenced by antagonist dose, with a continued effect 24 h after administration of the 500 micrograms/kg dose only. The maximum degree of LH suppression was 40% after 50 micrograms/kg (n = 6), 60% after 150 micrograms/kg (n = 6), and 59% after 500 micrograms/kg (n = 5). In contrast, plasma immunoreactive FSH levels did not change after these doses of the NAL-ARG GnRH antagonist. The maximum degree of FSH suppression was 16%, and the changes in plasma FSH concentrations were not dose dependent. Serum antagonist concentrations rose within 30 min after its administration to mean peak levels of 7.5 +/- 2.1 (+/- SE), 20.4 +/- 6.1, and 151 +/- 21 ng/mL after the 50, 150, and 500 micrograms/kg doses, respectively. The half-time of the disappearance of the NAL-ARG GnRH antagonist from plasma was 8.8 +/- 1.5 h. While there were no effects of antagonist administration on hematological, hepatic, or renal function, three women developed urticaria distant from the site of injection when administered the highest dose. We conclude that blockade of GnRH receptors by a GnRH antagonist 1) effectively antagonizes the action of GnRH, as assessed by its ability to block pulsatile LH secretion and reduce mean plasma LH levels; and 2) inhibits LH release to a considerably greater degree than FSH release, providing further evidence of possible GnRH-independent FSH secretion.

Adult↗
PubMed1986

[The effect of synthetic chicken LH-RH on the release of LH and FSH and ovulation in rats (a comparative study of synthetic mammalian LH-RH and chicken LH-RH)].

Recently, Miyamoto et al and King et al, independently isolated chicken LH-RH and determined its chemical structure as [Gln8] LH-RH. In this report, the in vivo effect of synthetic chicken LH-RH on the release of LH and FSH and ovulation in rats was investigated. A single i.v. injection of chicken LH-RH, as well as mammalian LH-RH, induced a significant increase of plasma LH levels at 15 min after injection in adult male rats. Plasma LH levels then declined at 30 min to 60 min and returned to basal levels at 120 min. The biological potency of chicken LH-RH estimated from plasma LH levels at 15 min after injection in adult male rats by parallel line assay was 4.1% of that of mammalian LH-RH. It was likely that the activity of chicken LH was shorter in duration on the LH secretion as compared with that of mammalian LH-RH because of quickly decreased plasma LH levels. Plasma FSH levels were also increased, but the increment of FSH was not so obvious as compared with that of LH. Plasma FSH levels reached a plateau at 15 min and did not return to basal levels at 120 min in either the chicken LH-RH injection groups or the mammalian LH-RH injection groups. The chicken LH-RH was able to induce an increase of plasma LH and FSH and ovulation in pentobarbital-blocked, proestrous female rats. The biological potency of chicken LH-RH estimated from plasma LH levels at 15 min after injection in pentobarbital-blocked, proestrous female rats was 2.2% that of mammalian LH-RH. The ovulation-inducing potency of chicken LH-RH estimated from ED50 was about 2.1% of that of mammalian LH-RH. It is noteworthy that chicken LH-RH has a LH and FSH releasing and ovulation inducing-activity on rats in vivo, but its biological potency is weaker and of shorter duration compared with that of mammalian LH-RH, although the chemical structure of chicken LH-RH is different from that of mammalian LH-RH.

Animals↗
PubMed1997

Stronger suppression of serum testosterone and FSH levels by a synthetic estrogen than by castration or an LH-RH agonist.

Serum levels of LH, FSH and testosterone (T) were measured by radioimmunoassays in 36 patients with advanced prostate cancer before and during androgen ablation therapies. Both leuprolide acetate (LH-RH agonist: LHRH-A) and diethylstilbestrol diphosphate (DES-DP) administration decreased serum LH significantly to an undetectable level (LHRH-A: P < 0.01, DES-DP: P < 0.05). LHRH-A and DES-DP diminished serum FSH to 20% of the pre-treatment level (P < 0.005) and to an undetectable level (P < 0.001), respectively. LHRH-A and DES-DP decreased serum T to the castration level and an undetectable level, respectively (P < 0.001). Serum levels of the same 3 hormones before and after DES-DP administration were measured in 8 patients who received DES-DP after LHRH-A treatment or castration because of relapse of the disease. DES-DP lowered serum FSH further than LHRH-A to an undetectable level (P < 0.005) and diminished T further than previous treatments to an undetectable level (P < 0.05 vs. LHRH-A, P < 0.01 vs. castration). These results suggest that 1) DES-DP is able to reduce T production from extra-testicular site(s), and achieve the minimal serum T level, and 2) this DES-DP action appears to be one of the mechanisms of the effectiveness of the estrogen on refractory prostate cancer after castration or LHRH-A. In addition, basal (independent of LH-RH) FSH secretion in elderly men is about 20% of total FSH secretion and DES-DP inhibits the basal FSH secretion at the level of the pituitary.

Aged↗
PubMed1978

The effect of prednisolone and metyrapone on FSH release induced by the administration of LRH.

The response of follicle-stimulating hormone (FSH) to a single injection of synthetic LRH was established in 7 and 6 women following an intramuscular dose of 0.2 mg and 0.1 mg. The secretion of FSH was greater in the group injected with 0.2 mg LRH than in the group injected with 0.1 mg. On the other hand, the response of FSH to a single injection of LRH (0.1 mg/subject) was established in 7 men before and after the pretreatment with metyrapone for one dat (4.5 g/subject). Pretreatment with metyrapone provoked a hypersecretion of FSH following a single injection of synthetic LRH. Seven women, 21--48 years of age who were treated with prednisolone for at least 1.5 months were examined for the responsiveness of the anterior pituitary to a single injection of synthetic LRH (0.2 MG). The secretion of FSH was not suppressed and the maximal serum level of FSH was observed 60 min after LRH injection.

17-Hydroxycorticosteroids↗
PubMed1988

Age-related changes in the secretory pattern of FSH and LH in response to LH-RH in prepubertal female rats.

Developmental changes in the pituitary responsiveness and the secretory pattern of FSH and LH in response to a single injection of LH-RH (100 ng/rat, s.c.) as estimated by increases in plasma concentrations of FSH and LH 10, 30 and 60 min after the injection were studied in female rats at 5, 10, 15, 20, 25 and 30 days of age. The pituitary responsiveness to LH-RH for both FSH and LH release increased from 5 to 15 days of age, reached a maximum on 15 days of age and declined thereafter, whereas a marked increase in the amount of these hormones in the pituitary occurred between 15 and 20 days of age. An apparent change in the secretory pattern of both FSH and LH was observed from 20 days of age onward. In groups up to 15 days of age, plasma concentrations of FSH and LH remained elevated 60 min after the injection of LH-RH, though the plasma concentration of these hormones returned to preinjection concentrations in groups at 20 days of age or later. These results indicate that the age-related changes in the secretory pattern of LH and FSH in response to LH-RH as well as changes in the pituitary responsiveness were apparent during the prepubertal period.

Age Factors↗
PubMed1976

Differences of the effects of testosterone propionate on the production of LH and FSH.

The effects of testosterone propionate (1 mg/day) on the synthesis and circulating levels of FSH and LH were studied in normal adult male rats. The pituitary and serum gonadotrophins were measured by double antibody radioimmunoassay. The de novo synthesis of gonadotrophins was assessed by the rate of in vitro incorporation of [3H]leucine into the immunoprecipitable FSH and LH. After 4 days of treatment with testosterone propionate the circulating LH levels dropped significantly, while FSH remained unchanged. Pituitary LH content and concentration declined significantly after 1 day, and incorporation of [3H]leucine into the immunoprecipitable LH became undetectable 4 days after initiation of treatment. Pituitary FSH content and concentration showed a significant increase after the 4th day of treatment. A slight tendency towards increased incorporation of [3H]leucine into FSH was observed throughout the treatment period, although it was statistically not significant. The data provide direct evidence for a differential effect of TP on FSH and LH production by the pituitary and show that the decrease in the pituitary and plasma levels of LH in testosterone treated rats is due to the decrease in LH synthesis.

Animals↗
PubMed1976

Serum LH and FSH levels following intravenous injection of a gonadotrophin releasing principle in normal and gonadectomized adult male rats treated with oestradiol-17beta or 5alpha-dihydrotestosterone.

Effect of intravenous administration of a synthetic gonadotrophin releasing factor (GnRF) on circulating LH and FSH concentrations was investigated in normal and gonadectomized, adult male rats injected subcutaneously each day during seven days with various doses of oestradiol-17beta or 5alpha-dihydrotestosterone in sesame oil. Higher increase in serum LH and FSH levels subsequent to intravenously administered GnRF was observed in castrated control animals than in intact control animals, though this increment was not of significant nature for serum FSH. Pre-treatment of normal and gonadectomized rats with oestradiol-17beta resulted in an augmented response of serum LH and FSH concentrations to GnRF iv. Pre-treatment of normal and gonadectomized rats with 5alpha-dihydrotestosterone diminished serum LH and FSH response following administration of the same amount of GnRF. For these steroids to affect the response pattern of serum LH and FSH to GnRF iv, higher doses were required in normal than in gonadectomized animals. The data indicate that oestrogen and androgen may act at different sites in the male hypothalamic-pituitary axis with respect to regulation of pituitary gonadotrophins.

Animals↗
PubMed1977

FSH: II. Evidence for its mediating role on testosterone secretion in hypopituitarism.

Testicular responses to administration of human chorionic gonadotrophin (HCG) in 23 hypopituitary patients were compared to responses obtained in adequate control groups and correlated to basal plasma follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels. Sixteen nonpubertal patients demonstrated a significantly diminished testosterone response (250 +/- 64 ng/100 ml, mean +/- SEM) along with low basal plasma FSH values (1.4 +/- 0.2 mU/ml) when compared to normal response (607 +/- 97 ng/100 ml) and normal FSH level (2.3 +/- 0.2 mU/ml), but with normal LH values. In 7 pubertal patients decreased testosterone responses to HCG (815 +/- 147 ng/100 ml) were observed with normal plasma FSH and LH values. Correlation between testosterone responses and FSH levels (r - 0.718, P less than 0.002) in the pre-pubertal hypopituitary patients was highly significant. No such correlation was observed between testosterone response and LH. The represent findings may a) give one explanation for the absence of response to HCG observed in some cases of hypopituitarism, b) give support to the hypothesis that FSH has a mediating role on LH-induced secretion of testosterone by the testis in human subjects.

Adolescent↗
PubMed1985

Divergent effects on LH and FSH synthesis and release from intact female rat pituitary glands in vitro by methylxanthines, cyclic AMP derivatives and sodium fluoride.

FSH release from the female rat pituitary gland consists of an LH-like, LRH-dependent component and an autonomous, inhibin-sensitive component. It was investigated whether cyclic AMP mediated FSH release. BrcAMP, theophylline, MIX or NaF stimulated LH release but inhibited FSH release and synthesis. Although dbcAMP had no inhibitory effect on FSH release, it partly reversed the inhibitory action of theophylline. In view of previous and the present results it is concluded that cyclic AMP may mediate the LRH-dependent LH and FSH release and, through a separate pathway, may mediate the inhibition of autonomous FSH release by the ovarian protein inhibin.

1-Methyl-3-isobutylxanthine↗