Fundamental to understanding the management of thyroid hormone - both in those who are healthy and in those who have thyroid disorders - is knowing what thyroid hormones actually do!
One of the first things I tried to look up when I became aware of thyroid issues was "What do they do?".
The answers I found were woolly - "control metabolism" seemed the most common sort of expression. But a severe lack of detail meant that we could not understand precisely which bits of our metabolism are controlled? Or exactly how.
Knowing the detailed effects, at the molecular level, should provide a route to understanding all the effects of impaired thyroid hormone management. And we might find many things we had never thought about become clear.
Molecules.2021 Dec; 26(23): 7337.
Published online 2021 Dec 3. doi: 10.3390/molecules26237337
PMCID: PMC8658769
PMID: 34885918
Main Factors Involved in Thyroid Hormone Action
Lorena Tedeschi,1 Cristina Vassalle,2 Giorgio Iervasi,1 and Laura Sabatino1,*
Raffaele Capasso, Academic Editor
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Abstract
The thyroid hormone receptors are the mediators of a multitude of actions by the thyroid hormones in cells. Most thyroid hormone activities require interaction with nuclear receptors to bind DNA and regulate the expression of target genes. In addition to genomic regulation, thyroid hormones function via activation of specific cytosolic pathways, bypassing interaction with nuclear DNA. In the present work, we reviewed the most recent literature on the characteristics and roles of different factors involved in thyroid hormone function in particular, we discuss the genomic activity of thyroid hormone receptors in the nucleus and the functions of different thyroid hormone receptor isoforms in the cytosol. Furthermore, we describe the integrin αvβ3-mediated thyroid hormone signaling pathway and its rapid nongenomic action in the cell. We furthermore reviewed the thyroid hormone transporters enabling the uptake of thyroid hormones in the cell, and we also include a paragraph on the proteins that mediate thyroid receptors’ shuttling from the nucleus to the cytosol.
Keywords: thyroid hormones, thyroid hormone receptor, integrin, genomic, nongenomic
Full paper freely accessible here:
ncbi.nlm.nih.gov/pmc/articl...
And this paper which cites the above paper:
Front Endocrinol (Lausanne).2021; 12: 803024.
Published online 2022 Jan 18. doi: 10.3389/fendo.2021.803024
PMCID: PMC8807339
PMID: 35126314
Inherited Disorders of Thyroid Hormone Metabolism Defect Caused by the Dysregulation of Selenoprotein Expression
Kyu Won Lee, 1 Yoochan Shin, 2 Sungahn Lee, 2 and Sihoon Lee
2 , *
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Abstract
Consistent activation and functioning of thyroid hormones are essential to the human body as a whole, especially in controlling the metabolic rate of all organs and systems. Impaired sensitivity to thyroid hormones describes any process that interferes with the effectiveness of thyroid hormones. The genetic origin of inherited thyroid hormone defects and the investigation of genetic defects upon the processing of thyroid hormones are of utmost importance. Impaired sensitivity to thyroid hormone can be categorized into three conditions: thyroid hormone cell membrane transport defect (THCMTD), thyroid hormone metabolism defect (THMD), and thyroid hormone action defect (THAD). THMD is caused by defects in the synthesis and processing of deiodinases that convert the prohormone thyroxine (T4) to the active hormone triiodothyronine (T3). Deiodinase, a selenoprotein, requires unique translation machinery that is collectively composed of the selenocysteine (Sec) insertion sequence (SECIS) elements, Sec-insertion sequence-binding protein 2 (SECISBP2), Sec-specific eukaryotic elongation factor (EEFSEC), and Sec-specific tRNA (TRU-TCA1-1), which leads to the recognition of the UGA codon as a Sec codon for translation into the growing polypeptide. In addition, THMD could be expanded to the defects of enzymes that are involved in thyroid hormone conjugation, such as glucuronidation and sulphation. Paucity of inherited disorders in this category leaves them beyond the scope of this review. This review attempts to specifically explore the genomic causes and effects that result in a significant deficiency of T3 hormones due to inadequate function of deiodinases. Moreover, along with SECISBP2, TRU-TCA1-1, and deiodinase type-1 (DIO1) mutations, this review describes the variants in DIO2 single nucleotide polymorphism (SNP) and thyroid stimulating hormone receptor (TSHR) that result in the reduced activity of DIO2 and subsequent abnormal conversion of T3 from T4. Finally, this review provides additional insight into the general functionality of selenium supplementation and T3/T4 combination treatment in patients with hypothyroidism, suggesting the steps that need to be taken in the future.
Keywords: thyroid, thyroid hormone, selenium, selenoprotein, deiodinase, genetics
Full paper freely accessible here:
Is thyroid my main issue?
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