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Summation of Basic Endocrine Data
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
To obtain the release of T3 and T4, there is proteolysis of thyroglobulin followed by endocytosis. Thyrotropin-releasing hormone (TRH), which is hypothalamic in origin, stimulates the pituitary to synthesize and release the thyroid-stimulating hormone (TSH). This promotes the uptake of iodide by the thyroid.
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
Thyroid heart disease in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Myron Miller, Steven R. Gambert
Through the action of the hypothalamic-releasing hormone (TRH), thyrotropin or thyroid-stimulating hormone (TSH) is released from the anterior pituitary and stimulates the release of thyroxine (T4) and triiodothyronine (T3) from the thyroid gland. In addition to a small amount of T3 made by the thyroid gland itself, T4 is converted to T3 by the thyroid gland and throughout the body in liver, muscle, and kidney tissue through enzymatic degradation by 5′-mono-deiodinase. T3 is the physiologically active cellular form of thyroid hormone and has both genomic and nongenomic actions to influence cardiac function by effects on stimulation of transcriptional processes and cellular membrane activity.
Thyroid functions as a parameter in monitoring of antiepileptic drugs
Published in Neurological Research, 2022
Ekim Comert, Ulufer Celebi, Bilge Piri Cinar, Mustafa Acikgoz, Esra Aciman Demirel, Huseyin Tugrul Atasoy
Many studies have been conducted on the negative impacts of AEDs on the hematological, endocrinological, and central nervous systems, as well as the ligaments of the body. The aim of this study was to evaluate the effects of antiepileptic therapy on thyroid function in epileptic patients. Synthesis of thyroid hormones takes place in the thyroid gland under the control of the hypothalamic–pituitary axis, and thyrotropin-releasing hormone produced by the hypothalamus stimulates TSH release from the hypophysis gland. T4 hormone is released from the thyroid gland and is converted into T3 hormone, which is a more active hormone with deiodinase enzyme in peripheral tissues [7]. T3 and T4 circulate through the blood in two forms: freely or bound. More than 99.8% of the thyroid hormone circulating in blood is bound to the plasma proteins thyroxine-binding globulin (TBG), transthyretin, and albumin. Less than 1% of the hormone in a free solution is in equilibrium with bound hormone [5].
RNA therapeutics for mood disorders: current evidence toward clinical trials
Published in Expert Opinion on Investigational Drugs, 2021
Marguerite Le Marois, Eleni Tzavara, El Chérif Ibrahim, Olivier Blin, Raoul Belzeaux
In a study published in 2015, Choi et al. [48] explored molecular mechanisms associated with the thyrotropin-releasing hormone (TRH) system underlying stress-induced depression. They found that RRS in mice persistently increased TRH and TRH receptor-1 (TRHR1) in the BLA, specifically in mice developing severe depressive-like behaviors, compared to resilient and control mice. They injected either TRH peptide or taltirelin – a TRH receptor agonist – directly in the BLA of non-stressed mice; both were sufficient to produce depressive-like behaviors. They next explored the signaling downstream of TRH receptor activation and identified p-ERK1/2 as a probable important mediator of the TRH receptor activation in the BLA involved in the stress-induced development of depressive-like behaviors.
Thyroid Feedback Quantile-based Index correlates strongly to renal function in euthyroid individuals
Published in Annals of Medicine, 2021
Sijue Yang, Shuiqing Lai, Zixiao Wang, Aihua Liu, Wei Wang, Haixia Guan
The secretion of thyroid hormone is regulated by hypothalamic-pituitary-thyroid (HPT) axis. Thyrotropin-releasing hormone (TRH) from the hypothalamus promotes the synthesis and release of TSH from the anterior pituitary, which plays an important role in all stages related to the production and secretion of thyroid hormones from the thyroid gland. The levels of TRH and TSH are in turn modulated by the negative feedback of thyroid hormones. Thyroid hormones are mainly secreted in the form of T4, which is catalyzed by deiodinases to form the bioactive T3. Both will bind to carrier proteins in the circulation and enter cells via membrane transporters. T3 then further binds to the nuclear thyroid hormone receptors. Therefore, thyroid function is regulated by the HPT axis and other factors associated with thyroid hormone conversion and bioactivity [26].