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Thyroid Hormones and Calcium Metabolism
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 functional units of the thyroid gland are the follicles (acini). They are made up of a single layer of cuboidal epithelial cells with a central lumen filled with colloid, which is predominantly a glycoprotein, thyroglobulin. Parafollicular cells (C cells), which secrete calcitonin, are scattered between the follicles. Thyroid hormone synthesis and release is regulated by a negative feedback by the hypothalamic–pituitary–thyroid axis. Thyroid-releasing hormone is released from the median eminence of the hypothalamus and transported to the anterior pituitary gland, where it stimulates the release of TSH.
Biochemistry
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
T3 and T4 synthesis and release are controlled and regulated by a classical ‘negative feedback system’. This involves reciprocal interactions between the thyroid gland and higher levels of control using information conveyed by circulating hormones. In this system, referred to as the hypothalamic−pituitary−thyroid axis, thyrotropin-releasing hormone (TRH) is secreted by the hypothalamic paraventricular nucleus into portal circulation, acting on the anterior pituitary thyrotropes to stimulate thyrothropin (thyroid-stimulating hormone, TSH) release. This subsequently acts via TSH receptors (TSHR) on thyroid follicular cells to stimulate cell proliferation as well as T4 and T3 synthesis and secretion [6,22,60,76].
BMI and Male Fertility
Published in Botros Rizk, Ashok Agarwal, Edmund S. Sabanegh, Male Infertility in Reproductive Medicine, 2019
Vinaya Gogineni, Ahmad Majzoub, Ashok Agarwal
Hormonal imbalance: Hyperthyroidism is a disorder in which too much thyroid hormone is produced; it has an association with oligospermia, abnormal sperm morphology, and infertility in men, and it provides an example of how the hypothalamic-pituitary-thyroid axis influences the HPG axis [19]. An increase in testosterone, seen in hyperthyroidism, prompts a negative feedback mechanism in which GnRH production and release is decreased, causing downstream effects on the HPG axis [14,51]. Research on the effect of hyperthyroidism on semen quality is rather sparse, but out of the studies that were conducted, most of the data signified findings of abnormal seminal parameters, specifically sperm motility [52]. Furthermore, for reasons that are not entirely clear, hyperthyroidism has been associated with erectile dysfunction and premature ejaculation, in addition to an increased amount of estrogen release [52–54].
Thyroid-disrupting effects of chlorpyrifos in female Wistar rats
Published in Drug and Chemical Toxicology, 2022
Joice Karina Otênio, Karine Delgado Souza, Odair Alberton, Luiz Rômulo Alberton, Karyne Garcia Tafarelo Moreno, Arquimedes Gasparotto Junior, Rhanany Alan Calloi Palozi, Emerson Luiz Botelho Lourenço, Ezilda Jacomassi
Several studies have shown that thyroid disruption might result from the inhibition of iodine intake in the thyroid gland by the sodium-iodide symporter, dysfunction of the hypothalamic-pituitary-thyroid axis, or an increase in the synthesis of uridine diphosphate glucuronyltransferase. These alterations may lead to the higher excretion of thyroid hormones (e.g., T3 and T4), lower cellular uptake, and the abnormal transcriptional activity of thyroid hormone receptors (Boas et al.2006, Jugan et al.2010). Most T3 is protein-bound, and total T3 levels may be affected by protein concentration or protein binding capacity (Mullur et al.2014). Thus, CPF at the highest dose tested in the present study may have affected binding with plasma proteins (e.g., thyroxine-binding globulin, thyroxine-binding prealbumin, and albumin), leading to higher free T3 levels. Although this is an interesting possibility, one limitation of our work was that we did not investigate the possible molecular mechanisms of this response profile or whether these changes are reversible after the cessation of CPF exposure.
Abdominal Obesity Phenotypes and Incidence of Thyroid Autoimmunity: A 9-Year Follow-up
Published in Endocrine Research, 2020
Atieh Amouzegar, Elham Kazemian, Hengameh Abdi, Safoora Gharibzadeh, Maryam Tohidi, Fereidoun azizi
A simultaneous rise in obesity and autoimmune disorders, including thyroid autoimmunity has been observed in the past decades.1,2 Several studies have demonstrated an association between thyroid autoimmunity and obesity. Some of these studies concluded that thyroid autoimmunity is the cause of hyperlipidemia and abdominal obesity rather than its consequence3 whereas others indicate that thyroid autoimmunity is the result of obesity. Leptin, an adipocytokine, has been proposed as a key factor in the development of thyroid autoimmunity in obese individuals.4–6 It is argued that obesity can impair thyroid function in different aspects such as activation of the hypothalamic–pituitary–thyroid axis and increased deiodinase activity.7–9 Changes in thyroid function tests in obese individuals are probably a result of obesity rather than its cause, since weight loss normalizes thyroid function tests.9
Therapeutic approaches of trophic factors in animal models and in patients with spinal cord injury
Published in Growth Factors, 2020
María del Carmen Díaz-Galindo, Denisse Calderón-Vallejo, Carlos Olvera-Sandoval, J. Luis Quintanar
TRH is a hypothalamic tripeptide with numerous physiological and biochemical actions. Its role in the hypothalamic-pituitary-thyroid axis is well known. TRH induces the synthesis and release of the thyroid stimulating hormone produced by the adenohypophysis, which in turn stimulates the thyroid gland for the synthesis and secretion of thyroid hormones (thyroxine and triiodothyronine) (Fröhlich and Wahl 2019). However, TRH or its analogous, may have neurological functions independent of thyroid hormones (Monga et al. 2008). Numerous preclinical studies have demonstrated that posttraumatic treatment of SCI with TRH or its analogues, improves of motor or sensitive functions. In patients with acute SCI with complete and incomplete injury groups within 12 h of trauma were treated with TRH (0.2 mg/kg intravenous bolus followed by 0.2 mg/kg/h infusion over 6 h). In these patients, clinical examination included motor and sensory testing, as well as assigning a Sunnybrook score based upon level of function. They were examined at 24 h, 72 h, 1 week, 1 month and 4 months after injury. There appeared to be no discernible treatment effect in patients with complete injuries although data were available from only six such patients at 4 months. For the incomplete injury group, a total of six treated and five placebo patients had 4-month evaluations. TRH treatment was associated with significantly higher motor, sensory, and Sunnybrook scores than placebo group (Pitts et al. 1995).