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Review
. 2011 May;34(5):395-407.
doi: 10.1007/BF03347465. Epub 2011 Mar 21.

Physiological role and regulation of iodothyronine deiodinases: a 2011 update

Affiliations
Review

Physiological role and regulation of iodothyronine deiodinases: a 2011 update

A Marsili et al. J Endocrinol Invest. 2011 May.

Abstract

T4 is a prohormone secreted by the thyroid. T4 has a long half life in circulation and it is tightly regulated to remain constant in a variety of circumstances. However, the availability of iodothyronine selenodeiodinases allow both the initiation or the cessation of thyroid hormone action and can result in surprisingly acute changes in the intracellular concentration of the active hormone T3, in a tissue- specific and chronologically-determined fashion, in spite of the constant circulating levels of the prohormone. This fine-tuning of thyroid hormone signaling is becoming widely appreciated in the context of situations where the rapid modifications in intracellular T3 concentrations are necessary for developmental changes or tissue repair. Given the increasing availability of genetic models of deiodinase deficiency, new insights into the role of these important enzymes are being recognized. In this review, we have incorporated new information regarding the special role played by these enzymes into our current knowledge of thyroid physiology, emphasizing the clinical significance of these new insights.

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Figures

Figure 1
Figure 1. Schematic representation of the deiodinase-mediated activation or inactivation of thyroxine and triiodothyronine
Figure 2
Figure 2. Mechanism for the incorporation of selenocysteine at the UGA Sec codon of selenoprotein mRNAs
When the ribosome encounters the in frame UGA codon its dissociation from the mRNA is inhibited and read through facilitated by a complex containing the specific selenoprotein charged tRNA, the selenoprotein specific elongation factor (EFsec) and the SECIS Binding Protein 2 (SBP2), all bound to the selenocysteine insertion-sequence (SECIS) element found in the 3’ untranslated region of all eukaryotic selenoprotein mRNAs. Modified from ref. (1)
Figure 3
Figure 3. Pathophysiology of the changes in the thyroid system during illness
Schematic representation of changes in circulating hormones with progressively more severe illness (A) and the effect on the deiodinases and TSH (B).

References

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