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Endocrine System
Published in Charles Paul Lambert, Physiology and Nutrition for Amateur Wrestling, 2020
Hormones are blood-borne substances released from one organ that circulate and stimulate biochemical reactions in another organ or organs (Guyton and Hall 2006). The hypothalamus is said to be the “commander in chief” of the endocrine system is the hormones and all of the organs and tissues involved in their release and uptake. The pituitary is said to be “the master gland” since it releases all of the stimulating hormones which stimulate the effector organs, and under most conditions, the pituitary is under the control of the hypothalamus. The hypothalamus receives input by the circulating levels of end hormones and under negative feedback homeostatic control mechanisms regulates the secretion of releasing hormones that go down to the pituitary. The pituitary will then put out stimulating hormones that are directed by the hypothalamus, which go to the effector organs and cause the release of the primary circulating hormone that goes to the blood and binds to target organs and DNA and effects metabolism or the biochemistry of the body. Two hormones are secreted directly by the posterior pituitary (Neurohypophysis) into the circulation, namely Oxytocin and ADH. All other hormones have a Releasing Hormone released by the hypothalamus that goes to the pituitary and cause the release of a Stimulating Hormone which acts at the effector organ to cause Primary Hormone release.
Influence of Ovarian Hormones on the Regulation of Luteinizing Hormone and Prolactin Release by Angiotensin II
Published in Craig A. Johnston, Charles D. Barnes, Brain-Gut Peptides and Reproductive Function, 2020
M.K. Steele, L.S. Myers, C.F. Deschepper, W.F. Ganong, K.N. Stephenson, R.L. Shackelford
The ovarian hormones also affect the activity of other brain peptides, like AII, neuropeptide Y, neurotensin, corticotropin releasing hormone, and oxytocin, which have been demonstrated to influence LH release. The “stimulatory” peptides may impinge upon the noradrenergic inputs to the LHRH neuron. Disrupting any one of these inputs, at least on an acute basis, will interfere with the LH surge and ovulation. However, reproductive success is a powerful physiological and behavioral drive. It is likely that, on a chronic basis, elimination of any one of these inputs would still be compatible with normal estrous cyclicity. The brain circuitry responsible for reproductive hormone release is probably redundant and can overcome disruption of any one “facilitatory” element.
Medical treatment of endometriosis
Published in Caroline Overton, Colin Davis, Lindsay McMillan, Robert W Shaw, Charles Koh, An Atlas of ENDOMETRIOSIS, 2020
Caroline Overton, Colin Davis, Lindsay McMillan, Robert W Shaw, Charles Koh
Gonadotropin releasing hormone agonists induce, stimulate and bind to the gonadotropin receptors on the anterior pituitary resulting in downregulation and a hypo-oestrogenic state. Following initial stimulation of the anterior pituitary and a ‘flare’ of gonadotropin release, gonadotropin levels are suppressed and the ovaries become inactive with resulting amenorrhoea.
Androgen-deprivation therapy and risk of death from cardio-vascular disease in prostate cancer patients: a nationwide lithuanian population-based cohort study
Published in The Aging Male, 2022
Justinas Jonušas, Mingailė Drevinskaitė, Aušvydas Patašius, Marius Kinčius, Ernestas Janulionis, Giedrė Smailytė
Androgen deprivation therapy (ADT) is a “backbone therapy” for patients diagnosed with advanced, metastatic, and high-risk localized prostate cancer [5]. There are several options of ADT, such as bilateral orchidectomy, gonadotropin-releasing hormone agonist (GnRH), and antagonist, with agonist used most widely. There are many studies on association between cardiovascular event incidence ratio and ADT. For example, Keating et al. showed that usage of gonadotropin-releasing hormone agonists increases the risk of coronary heart disease (HR 1.16, 95% CI [1.10–1.21]), myocardial infarction (HR 1.11, 95% CI [1.01–1.21]), and sudden cardiac death (HR 1.16, 95% CI [1.05–1.27]) [6]. The latest study by Cone et al. showed similar results – GnRH agonist usage increased the risk of heart failure and myocardial infarction (Odds ratio (OR) 2.06 (95% CI [1.76–2.41]) and 1.80 (95% CI [1.61–2.03]) respectively) [7]. On the other hand, the EORTC study reported no statistically significant difference between ADT users and non-users regarding cardiovascular diseases (CVD) [8].
Contribution of environmental factors and female reproductive history to hypertension and obesity incidence in later life
Published in Annals of Human Biology, 2022
Lenka Vorobeľová, Darina Falbová, Veronika Candráková Čerňanová
A study by Weihrauch-Blüher et al. (2019) considered the potential tracking of adiposity from early life and childhood to adulthood, and then the effect of increased adiposity in adolescence on earlier menarche onset. Further authors suggest that early-maturing girls could maintain their higher adiposity in adulthood (Must et al. 2005; Kivimèki et al. 2008), and Ahmed et al. (2009) added that leptin adipose tissue hormone has an important function in this process. This hormone signals the energy sufficiency which modulates the release of gonadotropin-releasing hormone from the hypothalamus. Therefore, serum leptin level in childhood is considered important in initiating the biological maturation process, menarche onset, and increased risk of non-communicable disease in later life (Ahmed et al. 2009; Mantzoros et al. 2009; Dreyfus et al. 2015).
Diabetes and mood disorders: shared mechanisms and therapeutic opportunities
Published in International Journal of Psychiatry in Clinical Practice, 2022
Laís Bhering Martins, Jenneffer Rayane Braga Tibães, Michael Berk, Antonio Lucio Teixeira
The HPA axis can be activated during acute and chronic stress responses (Steensberg et al. 2003). This activation generates the release of corticotropin-releasing hormone by the hypothalamus, which increases the synthesis and release of adrenocorticotropic hormone (ACTH) by the pituitary. ACTH, in turn, leads to increased production of adrenal cortisol (Joseph and Golden 2017). Although several factors can influence the activity of the HPA axis in MDD (e.g., severity of depressive symptoms, age, hospitalisation, and medication use), patients with MDD tend to have higher levels of cortisol and ACTH than non-depressive subjects (Stetler and Miller 2011; Joseph and Golden 2017; Jia et al. 2019). Cortisol causes an increase in the visceral adiposity and insulin resistance, which can favour the development of DM2 (Joseph and Golden 2017; Stalder et al. 2017; Nandam et al. 2019). Furthermore, patients with DM2 show variation in serum cortisol concentration and prolonged stress response (Geer et al. 2014), and HPA axis dysregulation by impaired CNS insulin signalling can favour the development of mood disorders (Lyra e Silva et al. 2019).