Cited by 23Thyroid Disorders and TreatmentsSelenium in Biological SystemsGrowth Hormone and Insulin-like Growth Factors

Iodothyronine deiodinases and reduced sensitivity to thyroid hormones

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Corsello, Salvatore Maria·2020·Frontiers in bioscience

Abstract

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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Crossref · 10.2741/4803

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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”
  • 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
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
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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