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At a Symposium held in Tokyo, Japan, on 21 and 22 May, 1987, entitled Inhibin–Non-steroidal Regulation of Follicle Stimulating Hormone Secretion it was proposed that the following definitions and nomenclature be adopted.
Inhibin is a glycoprotein hormone consisting of two dissimilar, disulphide-linked subunits, which inhibits pituitary gonadotrophin production and/or secretion, preferentially that of FSH. It was recommended that the nomenclature α and β, instead of A and B, be adopted for the subunits. The alpha subunit refers to the ∼ 20 kDa subunit of inhibin (31–32 kDa) which has been purified and cloned from porcine, bovine, ovine and human sources (Ling, Ying, Ueno et al. 1985: Mason, Hayflick, Ling et al. 1985; Miyamoto, Hasegawa, Fukuda et al. 1985: Rivier, Spiess, McClintock et al. 1985; Robertson, Foulds, Leversha et al. 1985; Forage, Ring, Brown et al. 1986; Fukuda, Miyamoto, Hasegawa et al. 1986; Mason, Niall & Seeburg, 1986, Mayo, Cerelli, Spiess
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ABSTRACT
Ovarian inhibin production is stimulated by the administration of human menopausal gonadotrophins or following a rise in endogenous LH and FSH. In order to determine whether FSH specifically stimulates inhibin secretion in vivo, immunoassayable serum inhibin levels were measured following the administration of a highly purified preparation of urinary FSH free of significant contamination with LH. Ten anovulatory women underwent a protocol of induction of ovulation with purified FSH and human chorionic gonadotrophin (hCG). During the induction of ovulation, blood samples were taken for radioimmunoassay of FSH, LH, oestradiol, progesterone and inhibin. During the administration of FSH there were increases in plasma concentrations of FSH, oestradiol and inhibin (P < 0·01) but no significant change in the concentration of LH. Oestradiol and inhibin concentrations rose in parallel and were closely correlated (τ = 0·920, n = 110, P < 0·001). There was also a direct correlation between the measured level of FSH and inhibin (τ = 0·512, n = 110, P < 0·05), but there was no correlation between LH and oestradiol, inhibin or FSH. Inhibin (τ− = 0·702, n = 10, P < 0·01) and oestradiol (τ− = 0·691, n = 10, P < 0·01) were correlated with the number of follicles seen on ovarian ultrasound. Levels of oestradiol and inhibin reached a peak on the day of hCG administration or on the following day. Inhibin levels then fell over the next 2 days in all cycles. In an ovulatory cycle resulting in conception, inhibin and oestradiol then rose in parallel with progesterone. We conclude that inhibin appears to be a follicular product which, in the follicular phase of the cycle, is stimulated by FSH alone, with granulosa cells being the probable site of production.
Journal of Endocrinology (1989) 122, 279–285
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SUMMARY
The presence of luteinizing hormone releasing factor (LH-RF) activity was investigated in pituitary stalk and systemic blood collected from rats ovariectomized at least 3 weeks previously, and in stalk blood from male rats in which electrodes had been implanted in the medial preoptic area of the brain. Most of the assayable luteinizing hormone (LH) present in the blood samples was eliminated by acid-ethanol extraction followed by ultrafiltration. The ultrafiltrates were injected into ovariectomized rats treated with oestrogen and progesterone, and increments in the concentration of LH in the sera of these animals, estimated by radioimmunoassay, were taken as an indication that the filtrate was able to release LH from the anterior pituitary gland. The ultrafiltrates of both the stalk and systemic plasma from the ovariectomized rats exhibited LH-RF activity as did the ultrafiltrates of blood collected from the pituitary stalk of the male rats during electrical stimulation of the preoptic area; stalk blood collected from these animals before the current was applied appeared to be inactive. The LH-RF activity of the ultrafiltrates of systemic and pituitary stalk plasma taken from ovariectomized rats was similar, and, therefore, the possibility is raised that the response of the pituitary glands in ovariectomized rats treated with oestrogen and progesterone is of an all or none type. The presence of appreciable quantities of LH-RF in the systemic plasma of ovariectomized rats may explain the discrepancy between bioassay and immunoassay estimates of LH in the plasma of these animals. The rapid increase in the concentration of serum LH and in the LH-RF activity of pituitary stalk plasma which followed stimulation of the preoptic area suggests that this region of the brain may be important in the control of the secretion of LH in the male as well as in the female animal.
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SUMMARY
The binding of 125I-labelled human growth hormone (HGH) to the 'lactogenic' binding sites of rat liver membranes has been shown to be highly dependent on the oestrogen and androgen status of the animal from which the membranes were prepared. Oestradiol treatment of either male or female rats induced a highly significant rise in HGH binding. The minimum effective dose used was 2–5 μg/day and the rise in HGH binding was apparent after 4 days of treatment. Following cessation of oestradiol treatment of male rats HGH binding declined with a half-time of approximately 9 days. In contrast to the stimulatory effect of oestrogen, treatment of female rats with testosterone propionate (minimum effective dose 100–200 μg/day) led to a marked reduction in HGH binding. The influence of both oestrogens and androgens was confirmed following the removal of endogenous sex steroids by adrenalectomy–ovariectomy of female rats and castration of male rats. Scatchard analysis showed that, with the possible exception of adrenalectomy–ovariectomy, all pharmacologically and physiologically induced changes in HGH specific binding reflected changes in binding site capacity; there were no changes in binding affinity. While earlier studies have indicated that the oestrogen effect is primarily indirect and is mediated by the pituitary gland, the mode of action of the androgens is currently unknown. The relatively slow response of HGH binding to hormonal changes would support an indirect action for both the sex steroids. The stimulatory effect of oestrogens and the inhibitory effect of androgens may provide an explanation for the marked sex difference in HGH binding to rat liver membranes.
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Concentrations of human growth hormone (HGH) in pituitary tumours measured by the tibial line assay (Young, Bahn & Randall, 1965) or assessed visually from electrophoretic patterns of pituitary extracts (Lloyd & Meares, 1965) have been shown to vary from quite low levels to concentrations greater than those present in the normal anterior pituitary gland. In the present study, HGH concentration in four normal anterior pituitary glands, obtained at autopsy, and in six pituitary tumours, resected surgically, has been estimated by radioimmunoassay and by inspection of starch-gel electrophoresis patterns. Histological examination of the tumour tissue was performed on paraffin sections of formalin-fixed specimens after staining with haematoxylin and eosin, eosin and methyl blue, and PAS-orange G. Extracts of pituitary tissue were prepared by homogenization in tris-EDTA-boric acid buffer at pH 8·9. The clear supernatant obtained after centrifugation was subjected to radioimmunoassay and to starch-gel electrophoresis. Radioimmunoassay was performed by the solid-phase
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SUMMARY
The paradoxical plasma growth hormone (GH) responses to oral glucose in certain patients with lung cancer prompted an examination of tumour extracts for GH releasing activity. Exposure of superfused rat pituitary to pulses (30 s) of aminophylline and to extracts from rat, sheep and human hypothalami resulted in a rapid and short-lived release of immunoreactive rat GH into the medium. Fresh extracts from five lung tumours, and from the surrounding lung tissue of four of these tumours significantly stimulated the release of GH, while extracts of a metastatic chondrosarcoma and normal rat lung were inactive. Gel filtration experiments suggested that the releasing activity in rat, sheep and human hypothalamic tissue and in human lung tumour extracts was present in at least two molecular species of different sizes.
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SUMMARY
Twenty-day-old male rats were injected intraperitoneally with either human luteinizing hormone (HLH) or human growth hormone (HGH) labelled with 125I. The localization of these hormones 1–2 hr. after injection was examined under the light microscope after radioautography.
Major sites of localization of labelled LH were the interstitial cells of the testis and the proximal convoluted tubule of the kidney. Some hormone was also present in adipose tissue, hepatic parenchymal cells, the mesothelial lining of the peritoneum and underlying macrophages. HGH was localized principally in the proximal convoluted tubule of the kidney with some hormone present in liver, adipose tissue, and the suprarenal cortex.
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ABSTRACT
The effects of 31 kDa bovine inhibin on the release of FSH and LH stimulated by gonadotrophin-releasing hormone (GnRH) or its agonist analogue buserelin have been studied using 5-day-old cultures of pituitary cells prepared from adult male Sprague–Dawley rats. Exposure of cultures to increasing concentrations of inhibin for 3 days before and during a 4-h stimulation with GnRH resulted in the progressive suppression of both basal and stimulated gonadotrophin release. At the highest inhibin concentrations FSH release was abolished (inhibin median inhibitory concentration (IC50) = 0·15 U/ml) whereas LH release was suppressed by 75% (IC50 = 0·93 U/ml). To correct for the reduced size of the FSH pool resulting from inhibin pretreatment, the amount of FSH or LH released by an agonist was expressed as a proportion of the total hormone available for release in each case. Following this adjustment, concentrations of inhibin producing maximal effects increased the GnRH median effective concentration for FSH release 4·1-fold and that for LH release 2·2-fold, with inhibin IC50 values of 0·45 and 0·32 U/ml respectively. Inhibin also suppressed the maximum proportion of both FSH and LH that excess GnRH released in 4 h by 36%, with IC50 values of 0·53 and 0·76 U/ml respectively. These effects were not changed by reduction of the inhibin pretreatment period from 3 days to 1 day or by exclusion of inhibin during the stimulation period. After a 3-day pretreatment, inhibin inhibited gonadotrophin release by buserelin less effectively than that by GnRH, but the pattern of antagonism was the same.
The results show that purified bovine inhibin antagonizes the release of both FSH and LH stimulated by either GnRH or buserelin in vitro by reducing the apparent potency of GnRH agonists and by decreasing the proportion of total available gonadotrophin that can be released by an excess of GnRH agonist. Higher concentrations of inhibin are required for these common actions against stimulated release of FSH and LH than for the inhibition of FSH tonic synthesis/basal release, indicating one or more secondary sites of inhibin action in addition to its primary selective action to suppress the constitutive synthesis of FSH.
J. Endocr. (1988) 119, 233–241
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ABSTRACT
We report inhibin α- and βA -subunit gene expression in the human corpus luteum and placenta using human α-subunit and bovine βA -subunit nucleic acid probes. In addition, we have demonstrated the presence of immunoreactive and bioactive inhibin in human corpora lutea. Our findings suggest that this tissue is a significant source of inhibin during the luteal phase of the normal human menstrual cycle.
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ABSTRACT
Serum concentrations of inhibin, FSH and LH were measured in 39 normal men and 127 men with testicular disorders resulting in infertility. The infertile men were divided into groups on the basis of their mean sperm count, FSH levels and karyotype. The mean (±s.d) serum concentrations of inhibin in the normal men was 554 ± 156 U/l and did not differ significantly from those groups with oligospermia, azoospermia or Klinefelter's syndrome. Combined analyses of all groups did not reveal any significant correlation between serum concentrations of inhibin and FSH or with any other parameter measured. Serum concentrations of FSH and LH were positively correlated, and Leydig cell dysfunction, as evidenced by increased serum LH levels, low testosterone levels or a declining testosterone/LH ratio were found with severe spermatogenic damage. The failure of serum concentrations of inhibin to correlate with those of FSH levels or the degree of testicular damage raise questions as to the clinical value of this parameter alone.
Journal of Endocrinology (1989) 120, 517–523
