Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases

Bianco, Antonio C.; Salvatore, Domenico; Gereben, Balázs; Berry, Marla J.; Larsen, P. Reed

doi:10.1210/edrv.23.1.0455

Cited by 1,853Thyroid Disorders and TreatmentsSelenium in Biological SystemsChemical Analysis and Environmental Impact

Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases

Bianco, Antonio C., Salvatore, Domenico, Gereben, Balázs, Berry, Marla J., Larsen, P. Reed·2002·Endocrine Reviews

DOI 10.1210/edrv.23.1.0455

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Abstract

The goal of this review is to place the exciting advances that have occurred in our understanding of the molecular biology of the types 1, 2, and 3 (D1, D2, and D3, respectively) iodothyronine deiodinases into a biochemical and physiological context. We review new data regarding the mechanism of selenoprotein synthesis, the molecular and cellular biological properties of the individual deiodinases, including gene structure, mRNA and protein characteristics, tissue distribution, subcellular localization and topology, enzymatic properties, structure-activity relationships, and regulation of synthesis, inactivation, and degradation. These provide the background for a discussion of their role in thyroid physiology in humans and other vertebrates, including evidence that D2 plays a significant role in human plasma T(3) production. We discuss the pathological role of D3 overexpression causing "consumptive hypothyroidism" as well as our current understanding of the pathophysiology of iodothyronine deiodination during illness and amiodarone therapy. Finally, we review the new insights from analysis of mice with targeted disruption of the Dio2 gene and overexpression of D2 in the myocardium.

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Due to alterations in rates of local deiodination in tissues, thyroid hormone signaling can change irrespective of serum hormonal concentrations.
“Due to alterations in rates of local deiodination in tissues, thyroid hormone signaling can change irrespective of serum hormonal concentrations (3, 5).”
From Can Reverse T3 Assay Be Employed to Guide T4 vs. T4/T3 Therapy in Hypothyroidism? (2019) · cites this paper as [3]
The D1 gene is upregulated by T3, and thus in hyperthyroidism the proportion of circulating T3 arising from the D1 pathway is significantly increased.
“Of note, the D1 gene is upregulated by T3, and thus in hyperthyroidism the proportion of circulating T3 arising from the D1 pathway is significantly increased (11).”
From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [11]
Type 3 deiodinase (D3) participates in the clearance of both serum T4 and T3.
“A third deiodinase, type 3 deiodinase (D3) participates in the clearance of both serum T4 and T3 (11).”
From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [11]
The insufficient peripheral T3 production cannot be appropriately corrected by increasing L-T4 dose, because the inhibitory effect of elevated T4 on D2 will end up increasing the imbalance of serum free T4 to free T3 ratio.
“The in-sufficient peripheral T3 production cannot be appropriately corrected by increasing L-T4 dose, because the inhibitory effect of elevated T4 on D2 [28,30,69] will end up increasing the imbalance of serum free T4 to free T3 ratio [67] .”
From 2012 ETA Guidelines: The Use of L-T4 + L-T3 in the Treatment of Hypothyroidism (2012) · cites this paper as [69]
The thyroid produces only about 5 mcg T3 daily.
“with the thyroid producing only ∼5 mcg T3”
From Liothyronine and Desiccated Thyroid Extract in the Treatment of Hypothyroidism (2020) · cites this paper as [32]

An additional about 25 mcg T3 is produced daily outside the thyroid parenchyma via T4 deiodination.
“an additional ∼25 mcg T3 is produced daily outside of the thyroid parenchyma via T4 deiodination (32).”
From Liothyronine and Desiccated Thyroid Extract in the Treatment of Hypothyroidism (2020) · cites this paper as [32]
Daily T3 production in a 70-kg healthy adult is about 30 mcg.
“The daily T3 production in a 70-kg healthy adult is ∼30 mcg”
From Liothyronine and Desiccated Thyroid Extract in the Treatment of Hypothyroidism (2020) · cites this paper as [32]
FT3 measurement has limited utility in the diagnosis of hypothyroidism because FT3 values often fall in the normal range due to hyperstimulation of remaining functioning thyroid tissue by elevated TSH and up-regulation of deiodinase D2.
“FT3 measurement has somewhat limited utility, however, in the diagnosis of hypothyroidism, since FT3 values often fall in the normal range as a result of hyperstimulation of the remaining functioning thyroid tissue by elevated TSH and to up-regulation of deiodinase D2”
From Diagnosis and management of treatment-refractory hypothyroidism: an expert consensus report (2017) · cites this paper as [25]
Deiodinases in central and peripheral tissues are regulated differently, enhancing T3 conversion and providing a differentiated mechanism for oversensitively responding to changes in FT4 in the feedback loop.
“Similarly, deiodinases in central and peripheral tissues are also regulated differently, enhancing T3 conversion and providing a differentiated mechanism for oversensitively responding to changes in FT4 in the feedback loop (55–63).”
From Homeostatic control of the thyroid-pituitary axis: perspectives for diagnosis and treatment (2015) · cites this paper as [57]
T3 supply is locally controlled by mechanisms including active thyroid hormone uptake, tissue-specific expression and activity of two distinct types of deiodinases converting T3 from T4, and thyroid hormone inactivation by deiodination or degradation.
“T3 supply is locally controlled by several mechanisms, such as active thyroid hormone uptake, tissue-specific expression and activity of two distinct types of deiodinases converting T3 from T4, and thyroid hormone inactivation by deiodination or degradation by sulfatation, deamination, or glucoronidation (57–66).”
From Homeostatic control of the thyroid-pituitary axis: perspectives for diagnosis and treatment (2015) · cites this paper as [57]
The brain predominantly expresses type 2 deiodinase, whereas type 1 deiodinase is abundant in other tissues of the body.
“The regulation varies by tissue as the brain predominantly expresses type 2 deiodinase, whereas type 1 deiodinase is abundant in other tissues of the body, and by thyroid state, as T3 excess upregulates type 1 deiodinase but downregulates type 2 deiodinase, which is upregulated in hypothyroidism (57–64).”
From Homeostatic control of the thyroid-pituitary axis: perspectives for diagnosis and treatment (2015) · cites this paper as [57]
T3 excess upregulates type 1 deiodinase but downregulates type 2 deiodinase.
“The regulation varies by tissue as the brain predominantly expresses type 2 deiodinase, whereas type 1 deiodinase is abundant in other tissues of the body, and by thyroid state, as T3 excess upregulates type 1 deiodinase but downregulates type 2 deiodinase, which is upregulated in hypothyroidism (57–64).”
From Homeostatic control of the thyroid-pituitary axis: perspectives for diagnosis and treatment (2015) · cites this paper as [57]
Type 2 deiodinase is upregulated in hypothyroidism.
“The regulation varies by tissue as the brain predominantly expresses type 2 deiodinase, whereas type 1 deiodinase is abundant in other tissues of the body, and by thyroid state, as T3 excess upregulates type 1 deiodinase but downregulates type 2 deiodinase, which is upregulated in hypothyroidism (57–64).”
From Homeostatic control of the thyroid-pituitary axis: perspectives for diagnosis and treatment (2015) · cites this paper as [57]
Conversion of T4 to T3 in the brain is catalyzed by D2.
“the conversion of T 4 to T 3 in the brain is catalyzed by D2 (94)”
From Central regulation of hypothalamic-pituitary-thyroid axis under physiological and pathophysiological conditions (2014) · cites this paper as [94]
In the cortex, hypothyroidism upregulates D2 activity to produce more T3, while hyperthyroidism downregulates D2 activity.
“In the cortex, for example, hypothyroidism up-regulates D2 activity to produce more T 3 , whereas hyperthyroidism down-regulates D2 activity (94)”
From Central regulation of hypothalamic-pituitary-thyroid axis under physiological and pathophysiological conditions (2014) · cites this paper as [94]
Deiodination of T4's outer ring by DIO2 gives T3, and deiodination of the inner ring by DIO1 or DIO3 gives reverse T3.
“Primarily, deiodination of T4’s outer ring by type 2 deiodinase (DIO2) gives liothyronine (L-tri-iodothyronine or T3, the main biologically active metabolite), and deiodination of the inner ring by type 1 or type 3 deiodinases (DIO1 or DIO3) gives the biologically inactive reverse T3 (rT3) [ 21 ].”
From Factors influencing the levothyroxine dose in the hormone replacement therapy of primary hypothyroidism in adults (2022) · cites this paper as [21]

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Distinct Subcellular Localization of Transiently Expressed Types 1 and 2 Iodothyronine Deiodinases as Determined by Immunofluorescence Confocal Microscopy
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Serum Triiodothyronine and Thyroxine in the Neonate and the Acute Increases in These Hormones Following Delivery
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Stereospecific transport of triiodothyronine from plasma to cytosol and from cytosol to nucleus in rat liver, kidney, brain, and heart.
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Concentrations of Thyroxine and 3,5,3′-Triiodothyronine at 34 Different Sites in Euthyroid Rats as Determined by an Isotopic Equilibrium Technique
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Inhibition of type I and type II iodothyronine deiodinase activity in rat liver, kidney and brain produced by selenium deficiency
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Retinoids stimulate type I iodothyronine 5'-deiodinase activity in human follicular thyroid carcinoma cell lines
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The Expression Pattern of Thyroid Hormone Response Genes in Remodeling Tadpole Tissues Defines Distinct Growth and Resorption Gene Expression Programs
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Comparison of Iodothyronine 5′-Deiodinase and Other Thyroid-Hormone-dependent Enzyme Activities in the Cerebral Cortex of Hypothyroid Neonatal Rat
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Estimation of thyroxine and triiodothyronine distribution and of the conversion rate of thyroxine to triiodothyronine in man.
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Peripheral tissue mechanism for maintenance of serum triiodothyronine values in a thyroxine-deficient state in man.
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The Role of Selenium in Thyroid Hormone Action*
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Characterization of the 5′-Flanking and 5′-Untranslated Regions of the Cyclic Adenosine 3′,5′-Monophosphate-Responsive Human Type 2 Iodothyronine Deiodinase Gene1
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Iodothyronine Metabolism in Liver and Kidney Homogenates from Hyperthyroid and Hypothyroid Rats*
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Effect of Acute Exposure to Cold on the Activity of the Hypothalamic-Pituitary-Thyroid System
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Thyroid Hormone Regulates Type I Deiodinase Messenger RNA in Rat Liver
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Selenocysteine tRNA [Ser]Sec Gene Is Ubiquitous within the Animal Kingdom
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Cloning and in vitro expression of the human selenoprotein, type I iodothyronine deiodinase
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Substitution of cysteine for selenocysteine in type I iodothyronine deiodinase reduces the catalytic efficiency of the protein but enhances its translation
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Interaction of Gold(I) with the Active Site of Selenium-Glutathione Peroxidase
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EFFECT OF SINGLE DOSE DEXAMETHASONE ON THE CONCENTRATION OF SERUM TRIIODOTHYRONINE IN MAN
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Production rates and turnover of triiodothyronine in rat-developing cerebral cortex and cerebellum. Responses to hypothyroidism.
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Acute Posttranscriptional Regulation of Cerebrocortical and Pituitary Iodothyronine 5′-Deiodinases by Thyroid Hormone*
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Comparison of the Biological Effects of Thyroxine and Triiodothyronine in the Rat*
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Sulfhydryl Groups and the Monodeiodination of Thyroxine to Triiodothyronine
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Timing of metamorphosis and the onset of the negative feedback loop between the thyroid gland and the pituitary is controlled by type II iodothyronine deiodinase in Xenopus laevis
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Optimal response of key enzymes and uncoupling protein to cold in BAT depends on local T3 generation
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Substrate-Induced Down-Regulation of Human Type 2 Deiodinase (hD2) Is Mediated through Proteasomal Degradation and Requires Interaction with the Enzyme’s Active Center1
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Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation
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“A third deiodinase, type 3 deiodinase (D3) participates in the clearance of both serum T4 and T3 (11).”
Management of Thyroid Dysfunction during Pregnancy and Postpartum: An Endocrine Society Clinical Practice Guideline
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Integrin αVβ3 Contains a Cell Surface Receptor Site for Thyroid Hormone that Is Linked to Activation of Mitogen-Activated Protein Kinase and Induction of Angiogenesis
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Iodine intake as a determinant of thyroid disorders in populations
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Early Life Exposure to Per- and Polyfluoroalkyl Substances (PFAS) and Latent Health Outcomes: A Review Including the Placenta as a Target Tissue and Possible Driver of Peri- and Postnatal Effects
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Reduced Activation and Increased Inactivation of Thyroid Hormone in Tissues of Critically Ill Patients
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Enzymatic Halogenation and Dehalogenation Reactions: Pervasive and Mechanistically Diverse
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Thyroid hormones in fetal growth and prepartum maturation
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Mutations in SECISBP2 result in abnormal thyroid hormone metabolism
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Hypothalamus‐Pituitary‐Thyroid Axis
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The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development
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Type 2 iodothyronine deiodinase is the major source of plasma T3 in euthyroid humans
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Authors: Bianco, A. C., Salvatore, D., Gereben, B., Berry, M. J., & Larsen, P. R.
Affiliations: Brigham and Women's Hospital (US)
Federico II University Hospital (IT)
Institute of Experimental Medicine, Hungarian Academy of Sciences (B.G.), Budapest, H-1083 Hungary
Corresponding author: Larsen, P. Reed
ORCID: Bianco, Antonio C.
Salvatore, Domenico
Berry, Marla J.
Venue: Endocrine Reviews
Publisher: The Endocrine Society
Published: 2002-02-01
Volume: 23
Issue: 1
Pages: 38-89
ISSN: 0163-769X (ISSN-L)
1945-7189
DOI: 10.1210/edrv.23.1.0455
OpenAlex: W2104878795
Cited by: 1,853
References: 531
Citations by year: 2026: 32 · 2025: 59 · 2024: 44 · 2023: 58 · 2022: 88 · 2021: 83 · 2020: 85 · 2019: 81 · 2018: 69 · 2017: 84 · 2016: 82 · 2015: 90 · 2014: 71 · 2013: 69 · 2012: 85
FWCI: 12.64
Type: journal article
Language: en
Open access: closed
Locations: Endocrine Reviews (publishedVersion)
PubMed (publishedVersion)
Funders: Brigham and Women's Hospital
National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK044128, DK36256, DK 58538, DK-44128, R01DK036256, T32DK007529, DK-07529)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
Health Sciences › Nursing › Nutrition and Dietetics › Selenium in Biological Systems
Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Chemical Analysis and Environmental Impact
Keywords: iodothyronine deiodinase, selenoprotein biosynthesis, type 2 deiodinase, type 3 deiodinase, type I deiodinase, thyroid hormone metabolism, structure-activity relationship
MeSH terms: Amino Acid Sequence, Animals, Base Sequence, Humans, Iodide Peroxidase, Molecular Sequence Data, Polymorphism, Genetic, Proteins, Protein Biosynthesis, Sequence Homology, Amino Acid, Selenoproteins

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Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases

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