ArticleEndocrinology2011
Distinct roles of deiodinases on the phenotype of Mct8 defect: a comparison of eight different mouse genotypes.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- 2024 European Thyroid Association Guidelines on diagnosis and management of genetic disorders of thyroid hormone transport, metabolism and action.European thyroid journal · 2024Guideline
- ExaminingFrontiers in toxicology · 2026Article
- Article
- A Genetically-Engineered Thyroid Gland Built for Selective Triiodothyronine Secretion.International journal of molecular sciences · 2025Article
- Toward a treatment for thyroid hormone transporter MCT8 deficiency - achievements and challenges.European thyroid journal · 2024Review
- Thyroid Hormone Transporters in Pregnancy and Fetal Development.International journal of molecular sciences · 2022Review
- Genetic disorders of thyroid development, hormone biosynthesis and signalling.Clinical endocrinology · 2022Review
- Genetic and Neurological Deficiencies in the Visual System ofInternational journal of molecular sciences · 2022Article
- Mathematical modeling and simulation of thyroid homeostasis: Implications for the Allan-Herndon-Dudley syndrome.Frontiers in endocrinology · 2022Article
- NovelThyroid : official journal of the American Thyroid Association · 2021Article
- Measurement of Reverse Triiodothyronine Level and the Triiodothyronine to Reverse Triiodothyronine Ratio in Dried Blood Spot Samples at Birth May Facilitate Early Detection of Monocarboxylate Transporter 8 Deficiency.Thyroid : official journal of the American Thyroid Association · 2021Article
- Thyroid Hormone Deiodinases: Dynamic Switches in Developmental Transitions.Endocrinology · 2021Review
- Human Type 1 Iodothyronine Deiodinase (Thyroid : official journal of the American Thyroid Association · 2021Article
- Monocarboxylate Transporter 8 Deficiency: From Pathophysiological Understanding to Therapy Development.Frontiers in endocrinology · 2021Review
- Intranasal delivery of Thyroid hormones in MCT8 deficiency.PloS one · 2020Article
- The relationship between inflammatory factors, oxidative stress and DIO-1 concentration in patients with chronic renal failure accompanied with or without euthyroid sick syndrome.The Journal of international medical research · 2018Article
- Sobetirome and its Amide Prodrug Sob-AM2 Exert Thyromimetic Actions in Mct8-Deficient Brain.Thyroid : official journal of the American Thyroid Association · 2018Article
- Regulation of T3 Availability in the Developing Brain: The Mouse Genetics Contribution.Frontiers in endocrinology · 2018Review
- Thyroid Hormone Signaling in the Development of the Endochondral Skeleton.Vitamins and hormones · 2018Review
- An Essential Physiological Role for MCT8 in Bone in Male Mice.Endocrinology · 2017Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Mice deficient in the thyroid hormone (TH) transporter Mct8 (Mct8KO) have increased 5'-deiodination and impaired TH secretion and excretion. These and other unknown mechanisms result in the low-serum T(4), high T(3), and low rT(3) levels characteristic of Mct8 defects. We investigated to what extent each of the 5'-deiodinases (D1, D2) contributes to the serum TH abnormalities of the Mct8KO by generating mice with all combinations of Mct8 and D1 and/or D2 deficiencies and comparing the resulting eight genotypes. Adding D1 deficiency to that of Mct8 corrected the serum TH abnormalities of Mct8KO mice, normalized brain T(3) content, and reduced the impaired expression of TH-responsive genes. In contrast, Mct8D2KO mice maintained the serum TH abnormalities of Mct8KO mice. However, the serum TSH level increased 27-fold, suggesting a severely impaired hypothalamo-pituitary-thyroid axis. The brain of Mct8D2KO manifested a pattern of more severe impairment of TH action than Mct8KO alone. In triple Mct8D1D2KO mice, the markedly increased serum TH levels produced milder brain defect than that of Mct8D2KO at the expense of more severe liver thyrotoxicosis. Additionally, we observed that mice deficient in D2 had an unexplained marked reduction in the thyroid growth response to TSH. Our studies on these eight genotypes provide a unique insight into the complex interplay of the deiodinases in the Mct8 defect and suggest that D1 contributes to the increased serum T(3) in Mct8 deficiency, whereas D2 mainly functions locally, converting T(4) to T(3) to compensate for distinct cellular TH depletion in Mct8KO mice.
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Registered trials
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