Minireview: Thyroid Hormone Transporters: The Knowns and the Unknowns
Open accessAbstract
The effects of thyroid hormone (TH) on development and metabolism are exerted at the cellular level. Metabolism and action of TH take place intracellularly, which require transport of the hormone across the plasma membrane. This process is mediated by TH transporter proteins. Many TH transporters have been identified at the molecular level, although a few are classified as specific TH transporters, including monocarboxylate transporter (MCT)8, MCT10, and organic anion-transporting polypeptide 1C1. The importance of TH transporters for physiology has been illustrated dramatically by the causative role of MCT8 mutations in males with psychomotor retardation and abnormal serum TH concentrations. Although Mct8 knockout animals have provided insight in the mechanisms underlying parts of the endocrine phenotype, they lack obvious neurological abnormalities. Thus, the pathogenesis of the neurological abnormalities in males with MCT8 mutations is not fully understood. The prospects of identifying other transporters and transporter-based syndromes promise an exciting future in the TH transporter field.
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TH needs to be taken up in cells by specific transporters including monocarboxylate transporter 8 (MCT8), monocarboxylate transporter 10 (MCT10) and organic anion transporting polypeptide family 1C1 (OATP1C1) to exert its action at the cellular level.
“In the past two decades it has become clear that TH needs to be taken up in cells by specific transporters including monocarboxylate transporter 8 (MCT8), monocarboxylate transporter 10 (MCT10) and organic anion transporting polypeptide family 1C1 (OATP1C1) to exert its action at the cellular level [1].”
From An update on non-thyroidal illness syndrome (2021) · cites this paper as [1]
These carriers appear to be necessary components of the feedback control, as simulated for IBS and demonstrated for MCT8 deficiency.
“These carriers appear to be necessary components of the feedback control, as simulated for IBS and demonstrated for MCT8 deficiency (27, 65).”
From Homeostatic control of the thyroid-pituitary axis: perspectives for diagnosis and treatment (2015) · cites this paper as [65]
T3 and T4 do not diffuse freely across the plasma membrane but are actively transported by specialized transport proteins such as MCT8, MCT10, and OATP1C1.
“Contrary to earlier assumptions, T3 and T4 do not diffuse freely across the plasma membrane but are actively transported by specialized transport proteins, such as MCT8, MCT10, and OATP1C1 (65).”
From Homeostatic control of the thyroid-pituitary axis: perspectives for diagnosis and treatment (2015) · cites this paper as [65]
T3 supply is locally controlled by mechanisms including active thyroid hormone uptake, tissue-specific expression and activity of two distinct types of deiodinases converting T3 from T4, and thyroid hormone inactivation by deiodination or degradation.
“T3 supply is locally controlled by several mechanisms, such as active thyroid hormone uptake, tissue-specific expression and activity of two distinct types of deiodinases converting T3 from T4, and thyroid hormone inactivation by deiodination or degradation by sulfatation, deamination, or glucoronidation (57–66).”
From Homeostatic control of the thyroid-pituitary axis: perspectives for diagnosis and treatment (2015) · cites this paper as [65]
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- Authors
- Visser, W. E., Friesema, E. C. H., & Visser, T. J.
- Affiliations
- Erasmus MC (NL)
- Corresponding author
- Visser, Theo J.
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2011-01-01
- Volume
- 25
- Issue
- 1
- Pages
- 1-14
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- PMC
- PMC5417302
- OpenAlex
- W1991454487
- Cited by
- 390
- References
- 101
- Citations by year
- 2026: 13 · 2025: 9 · 2024: 11 · 2023: 13 · 2022: 17 · 2021: 20 · 2020: 23 · 2019: 34 · 2018: 22 · 2017: 40 · 2016: 37 · 2015: 34 · 2014: 40 · 2013: 32 · 2012: 23
- FWCI
- 3.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Endocrinology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Chemical Analysis and Environmental Impact
- Keywords
- thyroid hormone transporters, thyroid hormones, MCT8, MCT10, OATP1C1, monocarboxylate transporters, organic anion transporting polypeptides, psychomotor retardation, neurological abnormalities
- MeSH terms
- Animals, Humans, Mutation, Thyroid Hormones, Monocarboxylic Acid Transporters
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