Regulation of Type 1 Iodothyronine Deiodinase in Health and Disease
Open accessAbstract
The major physiologic function of type 1 iodothyronine deiodinase (D1) is to produce triiodothyronine (T(3)) for the plasma. D1 activity is regulated by numerous factors, perhaps the most important of which in human pathophysiology is T(3). T(3) induces D1 expression, contributing to the T(3) excess commonly found in hyperthyroidism. Cytokines, nutritional status, sex steroids, and other factors also regulate D1 activity, although different organs often show different responses. Numerous homeostatic mechanisms can counterbalance isolated changes in D1 expression, such as the genetically decreased expression in C3H/He mice. Two relatively commonly used drugs, propylthiouracil and amiodarone, inhibit D1, which can have substantial effects on circulating thyroid hormone levels. Overall, many factors interact in complex ways to establish D1 levels, contributing to the circulating concentrations of thyroxine (T(4)) and T(3).
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T3 is the main stimulator of hepatic and kidney D1 activities through genomic actions.
“As T3 is the main stimulator of hepatic and kidney D1 activities (Koenig 2005, Gereben et al. 2008) through genomic actions, our results reinforce the idea of a T3-like genomic effect of 3,5-T2 on D1 regulation (rather than a non-genomic action).”
From Administration of 3,5-diiodothyronine (3,5-T2) causes central hypothyroidism and stimulates thyroid-sensitive tissues (2014) · cites this paper as Koenig 2005
The regulation of the D1 gene by T3 is mediated by the TRβ isoform.
“The regulation of the D1 gene by T3 is mediated by the TRβ isoform because T3 induction of hepatic and renal D1 is severely weakened in Thrb 1 (Thrb)-null mice but is normal in Thra 1 (Thra)-null mice (Koenig 2005).”
From Administration of 3,5-diiodothyronine (3,5-T2) causes central hypothyroidism and stimulates thyroid-sensitive tissues (2014) · cites this paper as Koenig 2005
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- Authors
- Koenig, R. J.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Koenig, Ronald J.
- ORCID
- Koenig, Ronald J.
- Venue
- Thyroid
- Publisher
- SAGE Publications
- Published
- 2005-08
- Volume
- 15
- Issue
- 8
- Pages
- 835-840
- ISSN
- 1050-7256 (ISSN-L)
- 1557-9077
- OpenAlex
- W2047401113
- Cited by
- 90
- References
- 5
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 6 · 2020: 1 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 5 · 2015: 9 · 2014: 4 · 2013: 3 · 2012: 3
- FWCI
- 0.68
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Locations
- Thyroid (publishedVersion)
- PubMed (publishedVersion)
- Deep Blue (University of Michigan) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK044155)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Surgery › Thyroid and Parathyroid Surgery
- Keywords
- type 1 iodothyronine deiodinase, triiodothyronine, thyroid hormone regulation, hyperthyroidism, cytokines, nutritional status, sex steroids, C3H/He mice, propylthiouracil, amiodarone, thyroxine, enzyme expression
- MeSH terms
- Animals, Circadian Rhythm, Eating, Feeding Behavior, Humans, Iodide Peroxidase, Liver, Mice, Inbred C3H, Selenium, Steroids, Thyroid Diseases, Thyroid Hormones, Triiodothyronine, Gene Expression Regulation, Enzymologic, Mice
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