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Measurement of Basal Metabolism
Published in Robert B. Northrop, Non-Invasive Instrumentation and Measurement in Medical Diagnosis, 2017
Other hormones can also produce high %BMR readings. These include adrenaline, anabolic steroids, and growth hormone, all of which stimulate metabolism. Certain neurosecretory endings in the median eminence of the hypothalamus release thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH), which in turn causes the thyroid gland cells to increase their output of TH and 3IT. High titers of circulating TH and 3IT inhibit the rate of secretion of TSH, providing feedback regulation of hormone concentration. Brain tumors that interrupt the TRH → TSH → TH pathway can lead to low TH and %BMR.
Hazard Characterization and Dose–Response Assessment
Published in Ted W. Simon, Environmental Risk Assessment, 2019
The secretion of TH by the thyroid is directly modulated by the action of thyroid-stimulating hormone (TSH). The paraventricular nucleus in the hypothalamus at the base of the brain produces thyrotropin-releasing hormone (TRH), a tripeptide, which is transported to the pituitary gland. TRH stimulates the pituitary gland to produce thyroid stimulating hormone (TSH) or thyrotropin, a 30 kD glycoprotein. TSH is released into the general circulation and stimulates the thyroid to produce TH.141 Secretion of both TRH and TSH is controlled by negative feedback from circulating TH.142
Endocrine system
Published in A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha, Clark’s Procedures in Diagnostic Imaging: A System-Based Approach, 2020
A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha
Release of thyroid hormones is under the control of the hypothalamus–pituitary axis. The hypothalamus produces thyrotrophin-releasing hormone (TRH), which causes the pituitary to release thyroid-stimulating hormone (TSH) that then stimulates the thyroid to release T3 and T4. A complex feedback mechanism maintains the correct blood levels of T3 and T4.
Urinary Isoflavones Levels in Relation to Serum Thyroid Hormone Concentrations in Female and Male Adults in the U.S. General Population
Published in International Journal of Environmental Health Research, 2021
Patricia A. Janulewicz, Jeffrey M. Carlson, Amelia K. Wesselink, Lauren A. Wise, Elizabeth E. Hatch, Lariah M. Edwards, Junenette L. Peters
Thyroid hormones (TH) are controlled through the hypothalamic-pituitary-thyroid (HPT) axis and are crucial for the regulation of many biological systems. The HPT axis is complex and sensitive to perturbations. The hypothalamus, located in the central nervous system, produces thyrotropin-releasing hormone (TRH), and sends it to the pituitary gland, which releases thyroid stimulating hormone (TSH). TSH binds to receptors on the thyroid gland and stimulates the synthesis and release of thyroid hormones, thyroxine (T4) and triiodothyronine (T3), into peripheral circulation. Proper production of these hormones is largely dependent on iodine levels (Rousset et al. 2000). Circulating TH levels are maintained by a feedback mechanism between the hypothalamus, pituitary gland, and thyroid gland (Rousset et al. 2000; Pearce and Braverman 2009; Gilbert et al. 2012). Optimal circulating TH levels are essential for normal fetal and child growth (Meeker 2012; DiVall 2013) and brain development (Meeker 2012), reproductive function, and metabolism (Meeker and Ferguson 2014).
Consumption of water contaminated by nitrate and its deleterious effects on the human thyroid gland: a review and update
Published in International Journal of Environmental Health Research, 2022
Edgar García Torres, Rebeca Pérez Morales, Alberto González Zamora, Efraín Ríos Sánchez, Edgar Héctor Olivas Calderón, José de Jesús Alba Romero, Esperanza Yasmín Calleros Rincón
It is the first endocrine gland developed in intrauterine life, and it begins functioning at 11–12 weeks of embryonic development (Sadler and Langman 2012). The thyroid follicle, formed by the circular union of thyrocytes, is the functional and structural part of the gland, which is composed of both follicular cells and C cells (Salgado et al. 2011). The TG requires iodine to synthesize and secrete thyroid hormones (THs), which have important roles in regulating physiology (De Escobar and Del Rey 2008; Ward 2012). THs include triiodothyronine, an active hormone known as T3, and thyroxine, a prohormone which is also known as T4. (Forrest and Visser 2013). The mechanism of regulation in THs synthesis occurs through a very finely tuned hypothalamic-pituitary-thyroid axis through which the hypothalamus generates thyrotropin-releasing hormone (TRH), which stimulates the synthesis and secretion of pituitary thyrotropin, also known as thyroid-stimulating hormone (TSH), which acts directly on the thyroid gland and initiates all the steps of the TH biosynthesis and secretion, this axis has a negative-positive feedback mechanism that can detect the presence of THs to maintain proper physiological levels of TRH and TSH in the body (Mendoza and Hollenberg 2017). THs have been described as influencing the following important physiological processes: cell proliferation and organism development, mainly throughout the embryonic stages; stimulation of the synthesis and degradation of proteins; and cell differentiation, THs are also required for the proper development of the central and peripheral nervous system during embryogenesis (Sadler and Langman 2012; Bursuk 2012). In addition, THs have been associated with energy metabolism, thermogenesis, the hepatic metabolism of nutrients, cardiovascular system function and the balance of corporal fluids (Ortiga‐Carvalho et al. 2016). To function correctly, the TG must have normal morphology and undergo normal biochemical processes, which require iodine, which enters the organism in the iodide form, and an adequate capacity to internalize it through the Na+/I− symporters (NISs) that are located in the plasma membranes of thyrocytes (Spitzweg and Morris 2002; De la Vieja et al. 2002; Bizhanova and Kopp 2009). These symporters are also present in other tissues, such as salivary glands, the small intestine and mammary glands (Chung 2014; Ravera et al. 2017). Any disruption in the synthesis of these hormones, in any stage of development, could lead to a malfunctioning of the entire organism (Chiovato et al. 2019).