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Embryology, Anatomy, and Physiology of the Male Reproductive System
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
FSH stimulates Sertoli cell proliferation and spermatogenesis.Stimulates the release of inhibin from the Sertoli cells.Inhibin affects the release of FSH from the pituitary gland through negative feedback.
Regulation of Reproduction by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The testes also produce several protein hormones that include activin, inhibin, and follistatin [26]. Inhibins are released into the blood and suppress pituitary FSH secretion, whereas activins mostly exert their actions as local paracrine/autocrine growth factors. Follistatin is a potent activin binding protein, which also modulates local biological functions. Inhibin is a dimeric glycoprotein existing in two bioactive forms: A and B. Inhibin B shows temporal changes in its expression with the changing role of the Sertoli cell in immature and adult testes. In the adult, the levels of inhibin B are positively correlated with sperm number and spermatogenic status and are negatively correlated with serum FSH levels. Production of inhibin B is regulated by complex interactions between FSH, Sertoli cells, Leydig cells, and germ cells. Inhibin may also play a role at autocrine or paracrine levels in modulating the actions of activin. Other compounds such as opioids, GnRH-like peptides, vasopressin, oxytocin, and several growth factors have also been detected in the testes and appear to function as paracrine agents.
The Use of Ovarian Markers
Published in Botros Rizk, Yakoub Khalaf, Controversies in Assisted Reproduction, 2020
Neena Malhotra, Siladitya Bhattacharya
Inhibin is structurally similar to AMH and belongs to the transforming growth factor (TGF)-β superfamily that selectively inhibits pituitary FSH release (21). It is now known that inhibin B is the dominant inhibin produced in the early and midfollicular phases, while inhibin A is the dominant inhibin synthesized in the late follicular and luteal phases of the menstrual cycle (21). Inhibin B was considered a candidate biomarker for ovarian reserve, and initial studies showed that concentrations of less than 45 pg/mL were associated with age above 35 years, poor response to gonadotropins, high cycle cancellation rates, reduced oocyte yield, and lower pregnancy rates (22,23). Most studies have demonstrated that inhibin B is not a good predictor of pregnancy (12,24). It exhibits high intracycle variability, and levels vary between menstrual cycles (25). Low inhibin B in the range of 40–45 pg/mL has specificity between 64% and 90% and sensitivity between 40% and 80%. The positive predictive value (PPV) of inhibin B is generally low (19%–22%) and negative predictive value (NPV) is high (95%–97%) in women undergoing IVF (26). In populations at high risk for DOR, PPV can be as high as 83% (27). In summary, the routine use of inhibin B as a measure of ovarian reserve is not recommended (1,12,24).
FSHR antagonists can trigger a PCOS-like state
Published in Systems Biology in Reproductive Medicine, 2022
Faiza Hanif Waghu, Karishma Desai, Sumana Srinivasan, Kaushiki S. Prabhudesai, Vikas Dighe, Kareenhalli V. Venkatesh, Susan Idicula-Thomas
Apart from CYP17A1 and LHCGR, inhibins are also reported to be differently expressed in women with PCOS. Inhibins are heterodimeric peptide hormones involved in hypothalamus-pituitary-ovarian axis that inhibit FSH secretion by the pituitary in phase-dependent manner. Inhibin A is predominantly secreted during the late follicular phase by granulosa cells of dominant follicle (de Kretser et al. 2002). Inhibin levels play a critical role in PCOS pathogenesis. In PCOS, due to aberrant folliculogenesis, the ovaries contain higher number of pre-antral follicles (Webber et al. 2003; Maciel et al. 2004). mRNA levels of Inhba were found to be significantly lower in follicles obtained from women with PCOS; indicative that insufficient inhibin secretion is associated with follicular arrest observed in PCOS (Fujiwara et al. 2001). Serum levels of inhibin A were significantly lower in women diagnosed with PCOS as compared to control group (Segal et al. 2010). We observed reduced mRNA levels of Inhba in ovaries of peptide-treated adult female rats as compared to ovaries of vehicle-treated rats (Figure 1). The results of gene expression analysis in toto indicated that administration of the FSHR antagonist peptide in adult female rats triggered a PCOS-like state. A limitation of the in vivo study is the use of small number of biological samples and restricted subset of genes known to be dysregulated in PCOS. The results will eventually have to be validated on a larger dataset to confirm the observations and obtain statistically significant results.
Endometrial development during the transition to menopause: preliminary associations with follicular dynamics
Published in Climacteric, 2020
A. Baerwald, H. Vanden Brink, C. Lee, C. Hunter, K. Turner, D. Chizen
The menopausal transition is a period of profound change in female reproductive physiology and menstrual cyclicity1. Gradual depletion of the ovarian reserve with age corresponds to a reduction in the number of antral follicles emerging for cyclic growth during each menstrual cycle2–4. A decrease in the number of preantral and antral follicles with age is thought to be related to a decrease in both anti-Müllerian hormone5–9 and inhibin B6,10,11. The loss of inhibin B-mediated feedback on pituitary gonadotropin production results in a rise in systemic follicle stimulating hormone (FSH)10–12. Luteinizing hormone (LH) concentrations rise gradually as women transition to menopause13,14. Luteal phase progesterone and follicular phase estradiol gradually decline during the menopausal transition, with the fall in estradiol being one of the last changes to occur6,15–18. Depletion of the ovarian reserve and resultant changes in hormone production may be accompanied by variability in menstrual cycle length19,20.
Plasma concentration of MMP-1 and MMP-2 in boys with cryptorchidism and its lack of correlation with INSL3 and inhibin B
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2019
Ewa Matuszczak, Marta Diana Komarowska, Anna Sankiewicz, Łukasz Ołdak, Ewa Gorodkiewicz, Wojciech Debek, Robert Milewski, Marzena Tylicka, Adam Hermanowicz
There is no biological explanation for the ‘special’ association between MMPs and inhibin B or INSL3. Inhibin B and INSL3 are major secretory products of Sertoli and Leydig cell, respectively. Inhibin B levels can reflect the status of the testis germinative epithelium, and levels of INSL3 can express the regulation of Leydig cells in the testes. During the process of descending to the scrotum, testicles are guided by the gubernaculum, which consists of mesenchymal cells and extracellular matrix, and MMPs are enzymes capable of remodeling of extracellular matrix, and modulate behavior of cells. According to Churchill gubernaculum’s maturation and also spermatogenesis, demand proper equilibrium of metalloproteinases and their inhibitors [5], thus we speculated that there could be a link between MMPs and inhibin B or INSL3.