Iodothyronine deiodinases and reduced sensitivity to thyroid hormones
Open accessAbstract
Iodothyronine deiodinases are selenoproteins that regulate thyroid hormone metabolism. Of the three types of deiodinases, type 2 is the major regulator of intracellular triiodothyronine concentration in both the hypothalamus and pituitary, and therefore the major regulator of thyrotropin secretion. A defect in iodothyronine deiodinase activity can lead to a reduced sensitivity to thyroid hormones action and the most recent literature includes these defects in the so-called “syndromes of reduced sensitivity to thyroid hormones”. To date, the pathogenic variants of the selenocysteine insertion sequence-binding protein 2 (SECISBP2) gene are the first and only inherited disorder of iodothyronine metabolism described. Moreover, there is a growing interest in understanding the possible role of polymorphisms of DIO1 and DIO2 genes in some pathological conditions and in determining the requirement of levothyroxine replacement and the role of combined levothyroxine-liothyronine therapy in carrying subjects affected by hypothyroidism and who need replacement therapy. Results on this topic are still conflicting and more studies are needed to assess the efficacy of combined levothyroxine-liothyronine replacement therapy in this subset of patients.
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Reduced activity of iodothyronine deiodinase type 1 or D2 can lead to altered sensitivity to thyroid hormones.
“Deficiency in the activity of iodothyronine deiodinase type1or D2 can result in altered sensitivity to thyroid hormones.67”
From Refractory hypothyroidism: unraveling the complexities of diagnosis and management (2023) · cites this paper as [67]
Loss-of-function polymorphisms in deiodinases have been proposed to contribute to failure of thyrotropin-guided LT4 therapy to completely abolish symptoms of hypothyroidism in some patients, due to insufficient provision of T3.
“Loss-of-function polymorphisms in deiodinases have been proposed to contribute to failure of thyrotropin-guided LT4 therapy to completely abolish symptoms of hypothyroidism in some patients, due to insufficient provision of T3”
From Pharmacodynamic and Therapeutic Actions of Levothyroxine (2021) · cites this paper as [134]
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- Authors
- Corsello, S. M.
- Affiliations
- Agostino Gemelli University Polyclinic (IT)
- Corresponding author
- Corsello, Salvatore Maria
- Venue
- Frontiers in bioscience
- Publisher
- IMR Press
- Published
- 2020
- Volume
- 25
- Issue
- 2
- Pages
- 201-228
- ISSN
- 1093-4715 (ISSN-L)
- 1093-9946
- DOI
- 10.2741/4803
- OpenAlex
- W2977458895
- Cited by
- 23
- References
- 0
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 4 · 2023: 3 · 2022: 4 · 2021: 5
- FWCI
- 1.83
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- cc-by-sa
- Locations
- Frontiers in bioscience (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Nursing › Nutrition and Dietetics › Selenium in Biological Systems
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Keywords
- iodothyronine deiodinase, selenoproteins, DIO1, DIO2, triiodothyronine, thyrotropin secretion, hypothyroidism, levothyroxine, liothyronine, genetic variants
- MeSH terms
- Humans, Hypothyroidism, Iodide Peroxidase, Isoenzymes, Mutation, Receptors, Thyroid Hormone, Thyroid Hormones, RNA-Binding Proteins, Hormone Replacement Therapy, Polymorphism, Single Nucleotide
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