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Endocrine Therapies
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
After secretion into the bloodstream, GnRH travels via the portal blood to the pituitary gland where it acts on its own receptor known as the Gonadotropin-Releasing Hormone Receptor (GnRHR), a seven-transmembrane G-Protein-Coupled receptor (Figure 8.24). This stimulates production of the beta-isoform of Phosphoinositide Phospholipase C, which then mobilizes calcium and Protein Kinase C. This results in the activation of proteins involved in the synthesis and secretion of the two pituitary hormones, Luteinizing Hormone and Follicle-Stimulating Hormone from the anterior pituitary. These hormones induce the production of estrogen and progesterone in the ovaries in females, and testosterone in the testes in males. This, in turn, induces ovulation in females and gametogenesis in males. GnRH is the target of various regulatory processes within the hypothalamic–pituitary–gonadal axis, and is inhibited by rising levels of estrogen or testosterone in females and males, respectively (i.e., via a feedback loop).
The Role of Gonadotropin-Releasing Hormone (GnRH) Agonists in the Treatment of Uterine Fibroids
Published in John C. Petrozza, Uterine Fibroids, 2020
Whitney A. Leonard, Alexander M. Quaas
Gonadotropin-releasing hormone (GnRH) is the primary hormonal stimulus of the hypothalamic-pituitary-gonadal axis. GnRH is produced in the arcuate nucleus of the hypothalamus and released to the hypophysial portal system, which connects the hypothalamus to the pituitary. GnRH then binds to the GnRH receptor on gonadotrophs in the anterior pituitary, stimulating the release of luteinizing hormone (LH), as well as follicle stimulating hormone (FSH), from the pituitary. These hormones then act on the ovaries to help control the menstrual cycle. Hormonal control of the reproductive organs has been utilized by the medical field to treat human disease and dysregulation of endocrine functions [1].
The endocrine system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
There are numerous causes of male infertility. Some are related to chromosomal defects, or to primary hypofunction of the hypothalamic–pituitary–gonadal axis. However, secondary changes in the hypothalamic–pituitary–gonadal axis may also be seen in diseases of other endocrine organs, and in chronic diseases of other organs, e.g. kidney and liver. Infertility may also follow on after medications, chemotherapy or exposure to toxic substances.
Re-determination of upper reference range of follicular stimulating hormone in infertile men
Published in Systems Biology in Reproductive Medicine, 2020
Muharrem Ozkaya, Unal Oztekin, Mehmet Caniklioglu, Oguz Ekmekcioglu
Follicular Stimulating Hormone (FSH) which is released with the stimulation of Gonadotropin-releasing Hormone (GnRH) and other factors, and whose secretion is modulated by glycoproteins such as Activin and Inhibin, is a peptide-structured hormone. It is secreted from the anterior part of the pituitary gland. FSH indicates the ability to produce sperm as a result of the feedback mechanism in the hypothalamic-pituitary-gonadal axis (HPGA) (Nieschlag et al. 1999; Tsutsui et al. 2010). Though the diurnal variability of FSH, a single serum FSH measurement shows the expected FSH value with great reliability. Hormonal assessment is also recommended as a part of the full evaluation in infertility. A high FSH level is an indicator of abnormal spermatogenesis and testicular insufficiency (Jarow et al. 2010).
Risk factors of gestational diabetes mellitus during assisted reproductive technology procedures
Published in Gynecological Endocrinology, 2020
Hu Shiqiao, Xu Bei, Zhang Yini, Jin Lei
In our study, we found fresh cycle transplantation may increase the risk of GDM which may due to the high level of circulating hormones. Some studied also showed that high E2 levels could destroy the endometrial receptivity which could influence the embryo implantation and subsequently impact the pregnancy outcomes. The exogenous sex hormones, GnRH and gonadotropins may affect hypothalamic–pituitary–gonadal axis and resulted in abnormal hormone levels which may increase the risk of GDM [14]. Royster et al. [26] thought high serum estradiol was a risk factors for adverse obstetric outcomes in ART through statistical analysis. However, Berntsen and Pinborg [27] supported that the risk of large for gestational (LGA) and macrosomia in frozen-thawed cycles was increased compared to fresh cycles. Meanwhile, Wei et al. [28] found frozen single blastocyst transfer was associated with a higher risk of pre-eclampsia, not associated with GDM. From our study, although fresh cycle transplantation may increase the risk of GDM, the incidence of GDM was increased among patients with the lower E2 level in the fresh cycle. E2 is secreted by granulosa cells which can reflect the quality of oocytes. During the process of ART in fresh cycle, E2 level was a positive correlation with the number of oocytes retrieved. After analysis E2 level of per oocyte, we found E2 level lower than 200 pg/mL can increase the risk of GDM. Therefore, it supported the quality of oocytes was associated with subsequently metabolism during pregnancy.
Current and potential targets for drug design in the androgen receptor pathway for prostate cancer
Published in Expert Opinion on Drug Discovery, 2018
Prostate cancer is the second most commonly diagnosed cancer in the USA with an estimated 161,360 new cases being diagnosed in 2017 [1]. While overall survival has improved for prostate cancer, an estimated 26,730 deaths will occur in 2017 [1]. Modulation of the androgen axis is an important part of management of prostate cancer. Androgen synthesis is tightly controlled by the hypothalamic-pituitary-gonadal axis. The pulsatile secretion of gonadotropin-releasing hormone drives the secretion of luteinizing hormone from the anterior pituitary gland which in turn stimulates the production of testosterone in the testes. The SRD5A2 isozyme of 5-alpha reductase is mostly responsible for the conversion of testosterone to dihydrotestosterone (DHT). This conversion is essential for the normal development of the prostate and deficiency of this enzyme may result in pseudohermaphroditism [2]. DHT is thought to play a greater role in androgen receptor (AR) signaling, as it is more potent than testosterone and DHT-receptor stability is greater than with testosterone [3,4].