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Pituitary Gland
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The gonadotropins, LH and FSH, are glycoproteins with two subunits, α and β. LH stimulates ovulation and luteinization of ovarian follicles in the female and testosterone secretion in the male. FSH stimulates the development of ovarian follicles and regulates spermatogenesis in the testes.
Neurohypophyseal Hormones and Reproductive Hormone Secretion
Published in Craig A. Johnston, Charles D. Barnes, Brain-Gut Peptides and Reproductive Function, 2020
The important physiological role which LH plays in the process of ovulation, and in the growth and maintenance of normal ovarian and testicular function is universally recognized (Dufau and Catt, 1978; Kulin and Reiter, 1973; Richards, 1980; Vaitukaitis et al., 1976). In fact, the severe clinical consequences resulting from the aberrant secretion of LH are well-documented and include hypogonadism, anovulatory menstrual cycles with resulting infertility, and several other physical and behavioral alterations (Illig et al., 1980; Skarin et al., 1982; Meldrum et al., 1982; Leyendecker et al., 1980; Liu et al., 1983; Marshall and Kelch, 1979). Furthermore, recognition of the important role that LH plays in regulating ovarian function and ovulation has resulted in a concentrated effort, by those developing successful oral contraceptive agents, to focus on inhibition of the preovulatory surge of LH as their endpoint in determining which therapies may represent potentially valuable contraceptive regimens (Diczfalusy, 1968). The magnitude and seriousness of clinical manifestations resulting from the aberrant secretion of LH, the frequency with which they occur in the normal population, and the proven therapeutic usefulness of altering plasma levels of LH to treat infertility or achieve contraception, make the elucidation of the neuroendocrine mechanisms controlling the secretion of LH very important.
Anatomy and physiology
Published in Suzanne Everett, Handbook of Contraception and Sexual Health, 2020
Menopause usually occurs in women between the ages of 45 and 55; the mean age in the UK is 48 years. The menopause is the permanent cessation of menses with loss of ovarian function. It is defined as 12 months of no menstruation, which can only be diagnosed retrospectively. During the menopause there is a deficiency of oestrogen and progesterone. The hypothalamus responds by increasing gonadotrophins. FSH and LH which can be ten times the normal menstruating woman’s levels. The reduction of oestrogen and progesterone and increase of follicle-stimulating and luteinizing hormones result in menopausal symptoms. Menopausal symptoms can vary between women, but women can complain of vaginal dryness, hot flushes or headaches. Women under the age of 50 should use contraception for two years after their last menstrual period, and women over the age of 50 should be advised to use contraception for one year after their last period (FSRH, 2010c).
Comparative study of DHEA and letrozole induced polycystic ovary syndrome in post-pubertal rats
Published in Gynecological Endocrinology, 2022
Patients with PCOS have hyperandrogenemia and are often associated with elevated serum AMH and an increased number of cystic follicles on ultrasound [22]. The intracytoplasmic AR input is caused by high androgen environment in blood circulation and local ovary, and the level of intracytoplasmic AR increases, which can lead to follicular development disorder, resulting in sparse ovulation or anovulation [23]. AMH in women is mainly secreted by granulosa cells in antral follicles [24]. The level of AMH is related to the number of antral follicles and is not affected by the menstrual cycle, and is often used to assess ovarian reserve function [25]. AMH reduces the sensitivity of follicles to FSH during follicular development and inhibits initial follicle recruitment and second retarding division. AMH reduces the sensitivity of follicles to FSH [26]. In PCOS patients, increased AMH inhibits FSH-dependent sinus follicle maturation, thus preventing the emergence of dominant follicles. In PCOS patients, changes in gonadotropin-releasing hormone lead to an increase in LH but a normal level of FSH, which leads to an increase in LH/FSH ratio [27]. High LH levels are closely related to endocrine disorders in the follicle, including increased androgen and insufficient estrogen aromatization caused by the relative decrease of FSH. Insufficient locally increased androgen binding estrogen leads to follicle growth stagnation [28].
Effects of vancomycin linoleic acid nanoparticles on male reproductive indices of Sprague–Dawley rats
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2021
Edwin Coleridge Stephen Naidu, Samuel Oluwaseun Olojede, Sodiq Kolawole Lawal, Aniekan Imo Peter, Edidiong Nnamso Akang, Onyemaechi Okpara Azu
The reduction in testosterone levels although not statistically significant in the VSLN group (F) compared to control animals may yet be of significance as the concentration of testosterone in the ST is normally markedly higher that the plasma concentration would suggest owing to the presence of specific androgen binding proteins found in the ST. The LH level were also notably significantly higher in the treatment groups when compared to controls suggesting alterations in the hypophyseal-pituitary gonadal axis. In males, LH stimulates interstitial cells to produce testosterone. Also, of note are FSH level which were also significantly reduced when compared to the controls. FSH acts directly on Sertoli cells. An elevated FSH level indicates abnormal spermatogenesis and may suggest impending testicular failure [50]. Azoospermia has been found in association with raised FSH and LH levels and a normal to low testosterone level [51]. These changes are relevant to findings in this study which suggest that the use of the preparations under study could lead to subfertility or frank infertility.
Current and experimental drug therapy for the treatment of polycystic ovarian syndrome
Published in Expert Opinion on Investigational Drugs, 2020
Luigi Della Corte, Virginia Foreste, Fabio Barra, Claudio Gustavino, Franco Alessandri, Maria Grazia Centurioni, Simone Ferrero, Giuseppe Bifulco, Pierluigi Giampaolino
The epigenetic evidence shows that testosterone, as well as glucose, are all active epigenetic modifiers of PCOS phenotypic expression that commonly includes both hyperandrogenism and glucose intolerance. Increased LH activity is a common feature in PCOS, and it may contribute to the defective folliculogenesis and hyperandrogenism commonly seen in these patients. Hypomethylation of LHCGR (that leads to increase gene expression) causes hypersensitivity to LH pulses, and thus it may be a plausible mechanism underlying susceptibility to PCOS [8]. Moreover, a genome-wide circulating miRNA expression profile identified several miRNAs dysregulated, mainly involved in glycometabolism and ovarian follicle development pathways. Interestingly, miRNA-592 is downregulated and inversely related to LHCGR levels in PCOS patients [14].