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Principles of Pathophysiology of Infertility Assessment and Treatment*
Published in Asim Kurjak, Ultrasound and Infertility, 2020
Joseph G. Schenker, Aby Lewin, Menashe Ben-David
Knobil observed that pulsatile secretion of Gn-RH is necessary to stimulate pituitary gonadotropin and to initiate and sustain ovulatory menstrual cycles in primates. An alteration in the pulsatile secretion of Gn-RH will cause an abnormality or cessation of the reproductive function.
Regulation of Reproduction by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
To function properly, GnRH has to be delivered in a pulsatile manner to the gonadotrophs, where it stimulates corresponding pulses of LH release [13]. The modulation of LH pulse frequency is essential for pubertal maturation as well as for a number of reproductive functions. In infancy, LH pulsatile secretion is transiently increased, likely reflecting pulsatile GnRH secretion, but soon becomes quiescent. The prepubertal suppression of the hypothalamo–pituitary–gonadal (HPG) axis occurs in agonadal humans and primates, suggesting that hypothalamo–hypophysial factors play a role in the postnatal quiescence of the reproductive axis, until puberty sets in. In women, the pattern of GnRH secretion is essential for the regulation of the menstrual cycle. LH pulse frequency is slow in the luteal phase but speeds up during the follicular and preovulatory phases, presumably reflecting changes in GnRH pulse frequency. Abnormalities in GnRH, and hence LH, pulse frequency, are associated with a number of reproductive endocrine disorders such as hypothalamic amenorrhea, hyperprolactinemia, and polycystic ovary syndrome (PCOS).
The Menstrual Cycle
Published in Jane M. Ussher, Joan C. Chrisler, Janette Perz, Routledge International Handbook of Women’s Sexual and Reproductive Health, 2019
Gonadotrophin-releasing hormone (GnRH) pulsatile secretion can be documented in peripheral blood as rhythmic peaks of the pituitary’s luteinizing hormone (LH). This integration involves insulin receptors (for adequacy of nutrition related to balance of caloric intake/expenditure), emotional signals (from the limbic system), hypothalamic temperature assessments (related to exercise, illness, and progesterone’s actions to raise core body temperature), assessment of sleep, as well as feedback from levels of the ovarian hormones (estrogen and progesterone).
Relevance and therapeutic implication of macroprolactinemia detection using PEG 6000 in women of childbearing age with hyperprolactinemia: experience at a tertiary hospital
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2023
Anne Ongmeb Boli, Martine Claude Etoa Etoga, Francine Mekobe Mendane, Charly Feutseu, Eloumba Mbono Samba, Amazia Falmata, Arnaud Manga Ndi, Jean-Claude Katte, Mesmin Dehayem, Vicky Jocelyn Ama Moor, Jean Claude Mbanya, Eugène Sobngwi
Prolactin (PRL) is a single-chain protein synthesised and released by lactotroph cells of the anterior pituitary gland.1 Its secretion is regulated by dopamine, which has an inhibitory effect on lactotroph cells.1 When prolactin secretion increases in the absence of pregnancy, clinical symptoms such as galactorrhoea and irregular menstrual cycles may occur. These menstrual abnormalities include spaniomenorrhoea and amenorrhoea, which may contribute to infertility. Hyperprolactinemia is a well-recognised hormonal aetiology of infertility among women of childbearing age. It affects 30–40% of infertile women and 15–20% of women with menstrual disorders.2 Impairment of gonadal function and, ultimately, infertility result from suppression of the pulsatile secretion of gonadotrophins.3 The majority of prolactin molecules present as monomers that are biologically active, but these may also exist as macromolecules (macroPRL) known as big and big-big prolactin, which may interfere with laboratory measurements of the protein.4 According to Vilar et al., in 2019, two Brazilian series reported macroPRL as the third cause of non-physiological hyperprolactinemia after drugs and pituitary adenomas.5 All three forms of prolactin are indistinguishable by routine laboratory assays.
Role of glucocorticoid negative feedback in the regulation of HPA axis pulsatility
Published in Stress, 2018
Julia K Gjerstad, Stafford L Lightman, Francesca Spiga
We have discussed the evidence for CORT-mediated negative feedback at the level of CRH and ACTH synthesis, as well as within the adrenal gland steroidogenic pathway. We have provided evidence from both mathematical modeling and experimental in vivo and in vitro studies, that pulsatility of ACTH and CORT is observed even with constant levels of CRH. This has challenged the long-standing hypothesis of a hypothalamic pulse generator-generating pulsatile CRH- to create downstream pulsatile secretion of ACTH and CORT. This suggests there must be a different role for the pulsatile pattern of CRH that has been observed in several species, including the rat. One possibility is that pulsatile CRH release is important for maintaining responsiveness of the pituitary–adrenal system. Indeed, it has been shown that sustained levels of CRH can result in a down regulation and desensitization of CRH receptors (Aguilera et al., 2004). CORT negative feed-back can of course still regulate CRH secretion and affect CORT pulsatility, as changes in the levels of CRH, both below and above physiological levels, will result in loss of ACTH and CORT pulsatility (Walker et al., 2010). How the pulsatile pattern of CRH modulates and interacts with the endogenously pulsatile pituitary–adrenal system is currently under active investigation.
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].