Dye, R. B., Rabinovici, J., & Jaffe, R. B. (1992). Inhibin and activin in reproductive biology. Obstetrical & gynecological survey, 47(3), 173-185. https://doi.org/10.1097/00006254-199203000-00014
Dye RB, Rabinovici J, Jaffe RB. Inhibin and activin in reproductive biology. Obstet Gynecol Surv. 1992;47(3):173-185. doi:10.1097/00006254-199203000-00014
Dye, R. B., et al. "Inhibin and activin in reproductive biology." Obstetrical & gynecological survey, vol. 47, no. 3, 1992, pp. 173-185.
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It has become apparent in recent years that regulation of the ovulatory cycle cannot be accomplished solely through the mediation of the two pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Within the last decade, discoveries of additional regulatory mechanisms involved in the neuroendocrine control of the events of the ovulatory cycle have provided new insight into the control of this complex biological phenomenon (127). Among the most interesting of these discoveries are …
Among 2,496 infertile Israeli women treated between 1964 and 1974, 143 cancer cases were observed as compared with 116.1 expected (standardized incidence ratio (SIR) = 1.2, 95% confidence interval (CI) 1.0-1.5) through 1991. Site-specific analysis revealed 12 ovarian cancers versus 7.2 expected (SIR = 1.6, 95% CI 0.8-2.9), 21 endometrial cancers versus 4.3 expected (SIR = 4.85, 95% CI 3.0-7.4), and 59 breast cancers versus 46.6 expected (SIR = 1.3, 95% CI 0.96-1.6). Sensitivity analysis revealed that confounding was unlikely to explain the raised risk of endometrial cancer, but nulliparity might explain the increased risk of ovarian cancer. The excess of endometrial cancer was prominent among patients with normal estrogen production but progesterone deficiency (SIR = 9.4, 95% CI 5.0-16.0). The risk for ovarian cancer was similar among the total groups of treated and untreated patients (SIR = 1.7 vs. 1.6). The standardized incidence ratio for endometrial cancer was higher among the treated group than the untreated group, although not significantly. Treatment with ovulation-inducing drugs does not appear to increase the risk for ovarian cancer, but its role cannot be completely excluded.
To explore the pulsatile-release characteristics of LH and P in women with premenstrual syndrome (PMS) compared with age-matched phase-matched controls. Prospective, repeated measures, two-group study. Human volunteers in an academic research environment. Six women with rigorously defined prospectively determined PMS; six age-matched phase-matched controls. Frequency, amplitude, concentration, and coincident pulsatile release characteristics of LH and P at three symptom-related points of the luteal phase. No significant between-group differences in frequency, amplitude, or concentration were found. In pooled data, significant coincident pulsing between LH and P was demonstrated. The length of time between LH and P pulses systematically increased across the luteal phase, a finding not previously reported. In the PMS group only, significant coincident pulsing occurred at an unexpected zero time lag on the symptom-onset sampling day. A progressively increasing coupling interval may reflect the gradual decline of the corpus luteum. Presence of a zero time lag between LH and P at symptom onset in women with PMS may indicate an aberrance in corpus luteum response to LH stimulation.
This study was designed to investigate the effect of varying concentrations of estradiol, administered to normal women, upon the gonadotropin response to synthetic gonadotropin-releasing hormone (GnRH or LRF). Beginning at 4 pm on the first day of the menstrual cycle, 19 studies were performed in subjects who received injections of estradiol benzoate (E2B every 12 h for 6 days). Concentrations of E2B administered (mug/kg/12 h) were: 0.3, 0.6, 1.25, 2.5, 3.75, and 5.0. Mean serum estradiol concentrations achieved at these respective concentrations of E2B were 43, 53, 91, 145, 195, and 305 pg/ml. Twelve h after the last E2B injection, an intravenous bolus of 100 mug GnRH was administered. Gonadotropin response to this dose of GnRH after E2B was compared with each subject's response in the early follicular phase of a previous (control) cycle during which no exogenous estradiol was administered.
This chapter has presented a somewhat complex view of the gonadotrope population, indicating that it consists of independent subsets. There may be regulatory cells that influence development and other ancillary processes needed for normal reproduction. For example, normal differentiation of PRL cells requires a functioning population of gonadotropes (Kendall et al., 1991). In addition, gonadotropes appear to be autoregulatory; subsets may produce inhibin or activin (in rats) and follistatin. Production of GnRH itself may serve as another regulatory tool. The gonadotrope population appears to be quite dynamic and convertible in the female rat. Cytological and cytochemical changes with the stage of the cycle are obvious. Increases in the numbers of immunoreactive gonadotropes parallel increases in GnRH target cells and culminate in peak expression of LH and FSH beta subunit mRNAs. The immunoreactive gonadotropes are greatly reduced after the surge activity, as though the cells had disappeared from the population. However, gonadotropes can still be detected by their content of gonadotropin mRNAs. This finding has led to the hypothesis that the gonadotropes recycle themselves. However, do they go through a resting phase? Is there a normal cycle of cell death and turnover? These are basic questions that must be answered in order to understand how the population is organized and renewed. Finally, we have returned to one of our original problems. Whereas it is clear that nonparallel release can be brought about by granules or cells with only one gonadotropin, the exact mechanisms that sort the gonadotropin molecules or turn off bihormonal expression are not known. A combination of autoregulatory events involving follistatin, activin, inhibin, and possibly steroids may play a role in modulating expression by a given subset. Delays in maturation may also prevent secretion of FSH and, hence, effect the delayed rise seen during late proestrus. The nonsecretory FSH cells seen in the studies by Lloyd and Childs (1988a) may be delayed maturers, requiring additional receptor types or changes in the calcium flux pattern to secrete their product. We also have a new question to address. What is the significance of the presence of GH in proestrous gonadotropes? Is GH a regulatory hormone, bound to receptors inside gonadotropes, or do subsets of somatotropes augment the population, producing a cocktail of GH and gonadotropins to aid ovulation? Either hypothesis is intriguing. Co-storage of GH and gonadotropins would be an efficient way of providing the hormones needed by the ovary. However, further work with in situ hybridization is needed to detect GH mRNA in such cells.(ABSTRACT TRUNCATED AT 400 WORDS)
Meunier H et al., 1988·Proc Natl Acad Sci U S A·Free full text on PubMed Central
The S1-nuclease analysis was used to investigate the pattern of inhibin expression in the rat. In a first series of experiments, expression of the alpha, beta A, and beta B subunits of inhibin were monitored in various tissues from male and female rats. Two observations emerge from these studies. First, expression of inhibin subunits was found in gonadal and extragonadal tissues. In addition to the ovary and testis, inhibin alpha, beta A, and beta B RNAs were detected in the placenta, pituitary, adrenal, bone marrow, kidney, spinal cord, and brain. Detection of inhibin RNAs in the brain and spinal cord suggested that these subunits may exert neuroregulatory functions in the central and peripheral nervous systems. Furthermore, the presence of inhibin alpha and beta subunits in the placenta and the pituitary gland, two cell types that have clearly been shown to be regulated by exogenous inhibin, may reflect existing paracrine and/or autocrine processes active in these tissues. The second observation is that expression of inhibin subunit RNAs may vary by severalfold in a tissue-specific fashion. for example, alpha-subunit RNA levels are abundant in the gonads, whereas beta A-subunit RNA is predominant in the placenta and bone marrow. Finally, it is noted that expression of testicular inhibin RNA subunits decreases during sexual maturation. We conclude that the dimers comprised of inhibin subunits possess diverse functions and may act as growth/differentiation factors as well as a hormone.
Yong PY et al., 2003·Human reproduction (Oxford, England)
Analyses of the follicular reserve and activity of the ovary are central to our understanding of the regulation of follicular development. We have carried out a prospective analysis of endocrine and biophysical assessments under three differing basal conditions: the early follicular and mid-luteal phases, and following GnRH analogue down-regulation. Hormonal analyses were carried out before and after a single dose of FSH on spontaneously ovulating women (n = 58). Ovarian volume and antral follicle count (AFC) were also determined. Inhibin B and estradiol concentrations were increased by FSH under all three conditions, and inhibin A in the follicular phase and after down-regulation. Basal hormone concentrations, except inhibin A and B after down-regulation, did not generally correlate with AFC. A close relationship between inhibin B and AFC was evident at all stages after FSH administration (r = 0.70-0.77). AFC and inhibin B after FSH stimulation were well correlated with the number of oocytes recovered after superovulation. Multivariate analysis demonstrated that inhibin B after FSH administration in the down-regulated state showed the closest correlation with oocyte number. In the more clinically useful early follicular and luteal phases, basal FSH was the most significant contributor to the number of oocytes, with a significant contribution from luteal phase AFC. These data extend our understanding of the relationships between follicular number, follicular functional activity, and the recruitable follicular population. Down-regulation and subsequent FSH stimulation was required to clearly demonstrate the close relationship between inhibin B and the ovarian reserve. Without such complex manipulation, early follicular phase FSH (supplemented by AFC in the relatively hypogonadotrophic luteal phase) remains of greater value in predicting the ovarian reserve than the currently known direct products of the ovary.
In rhesus monkeys with hypothalamic lesions (which appear to abolish the endogenous production of gonadotropin-releasing hormone), normal ovulatory mestrual cycles were reestablished by an unvarying, long-term replacement regimen consisting of one intravenous pulse of synthetic gonadotropic-releasing hormone per hour. This finding is in accord with the hypothesis that the pattern of pituitary gonadotropin secretion throughout the menstrual cycle (basal secretion interrupted, once every 28 days on the average, by a preovulatory surge) is not directed by alterations in hypothalamic gonadotropin-releasing hormone secretion but by the ebb and flow of ovarian estrogens acting directly on the pituitary gland.
PMID 1741100 1741100 DOI 10.1097/00006254-199203000-00014 10.1097/00006254-199203000-00014 Dye et al. 1992, Dye 1992
Cite this article
Dye, R. B., Rabinovici, J., & Jaffe, R. B. (1992). Inhibin and activin in reproductive biology. Obstetrical & gynecological survey, 47(3), 173-185. https://doi.org/10.1097/00006254-199203000-00014
Dye RB, Rabinovici J, Jaffe RB. Inhibin and activin in reproductive biology. Obstet Gynecol Surv. 1992;47(3):173-185. doi:10.1097/00006254-199203000-00014
Dye, R. B., et al. "Inhibin and activin in reproductive biology." Obstetrical & gynecological survey, vol. 47, no. 3, 1992, pp. 173-185.
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