Reawakened interest in type III iodothyronine deiodinase in critical illness and injury
Open accessAbstract
Thyroid hormones influence gene expression in virtually all vertebrate tissues. Precise regulation of the active endogenous ligand, 3,5,3'-triiodothyronine (T(3)), is achieved by the sequential removal of iodine moieties from the thyroid hormone molecule. Type III iodothyronine deiodinase (D3) is the major inactivating enzyme terminating the action of T(3) and preventing activation of the prohormone, thyroxine (T(4)). Recent studies have revealed the induction of high D3 activity in diverse animal models of tissue injury including starvation, cryolesion, cardiac hypertrophy, infarction, and chronic inflammation. By analyzing serum and tissues taken from hospitalized patients at the time of death, investigators have also documented the robust induction of D3 activity in several human tissues that normally have none, including the liver and skeletal muscle, and shown clinically relevant consequences to systemic thyroid status. These studies reveal a novel role of D3 in the tissue response to injury and in the derangement of thyroid hormone homeostasis commonly observed during critical illness.
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In disease states, particularly hypoxic states, D3 expression can be found ectopically in a wide range of tissues; the resultant increase in T3 clearance promotes tissue-specific and systemic lowering of T3 and has been implicated in the pathogenesis of nonthyroidal illness syndrome.
“In disease states, and particularly in hypoxic states, D3 expression can be found ectopically in a wide range of tissues (26); the resultant increase in T 3 clearance promotes both tissue-specific and systemic lowering of T3 and has been implicated in the pathogenesis of the ''nonthyroidal illness syndrome'' (27).”
From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [27]
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Experimental — accuracy not yet measuredHypothyroidism can result from accelerated clearance of thyroid hormones beyond what the thyroid gland can compensate for by increasing thyroid secretion.
“It can also be the result of accelerated clearance of TH, beyond what the thyroid gland can compensate for by increasing thyroid secretion (2).”
From Emerging Therapies in Hypothyroidism (2024) · cites this paper as [2]
Elevation of systemic inflammation such as during injury, inflammation, or starvation leads to the non-thyroidal illness syndrome, which has features including downregulation of hypothalamic thyrotropin-releasing hormone, lowered secretion of TSH, free T4, and free T3, decreased levels of circulating free T3 due to decreased peripheral T4→T3 conversion, and increased metabolism of biologically活跃 T
“Elevation of systemic inflammation such as during injury, inflammation, or starvation leads to the non-thyroidal illness syndrome, which has the following features [131]: (a) downregulation of hypothalamic thyrotropin-releasing hormone; (b) lowered secretion of TSH, free T4, and free T3; (c) decreased levels of circulating free T3 due to decreased peripheral T4→T3 conversion; and (d) increased”
From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [131]
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- Authors
- Huang, S. A., & Bianco, A. C.
- Affiliations
- Harvard University (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Bianco, Antonio C
- Venue
- Nature Clinical Practice Endocrinology & Metabolism
- Published
- 2008-01-22
- Volume
- 4
- Issue
- 3
- Pages
- 148-155
- ISSN
- 1745-8366 (ISSN-L)
- 1745-8374
- PMC
- PMC3133953
- OpenAlex
- W2067881527
- Cited by
- 95
- References
- 67
- Citations by year
- 2026: 1 · 2025: 6 · 2023: 3 · 2022: 1 · 2021: 5 · 2020: 4 · 2019: 5 · 2018: 4 · 2017: 4 · 2016: 10 · 2015: 8 · 2014: 10 · 2013: 5 · 2012: 8
- FWCI
- 0.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Clinical Practice Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- CYTED Ciencia y Tecnología para el Desarrollo
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK058538, DK 65055, DK77148, R56DK058538, R01DK065055, DK 58538, DK76099, R01DK077148, R01DK076099)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Keywords
- thyroid hormone inactivation, triiodothyronine, thyroxine, critical illness, tissue damage, thyroid hormone homeostasis, trauma response, myocardial infarction, cardiac hypertrophy, chronic inflammation, starvation, cryolesion, skeletal muscle, liver, hospitalized patients
- MeSH terms
- Animals, Euthyroid Sick Syndromes, Humans, Iodide Peroxidase, Thyroid Hormones, Wounds and Injuries, Critical Illness
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