Cited by 318Thyroid Disorders and TreatmentsDrug Transport and Resistance MechanismsChemical Analysis and Environmental Impact

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Tissue-Specific Thyroid Hormone Deprivation and Excess in Monocarboxylate Transporter (Mct) 8-Deficient Mice

Dumitrescu, Alexandra M., Liao, Xiao-Hui, Weiss, Roy E., Millen, Kathleen, Refetoff, Samuel·2006·Endocrinology

DOI 10.1210/en.2006-0390

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Abstract

Mutations of the X-linked thyroid hormone (TH) transporter (monocarboxylate transporter, MCT8) produce in humans unusual abnormalities of thyroid function characterized by high serum T3 and low T4 and rT3. The mechanism of these changes remains obscure and raises questions regarding the regulation of intracellular availability and metabolism of TH. To study the pathophysiology of MCT8 deficiency, we generated Mct8 knockout mice. Male mice deficient in Mct8 (Mct8(-/y)) replicate the thyroid abnormalities observed in affected men. TH deprivation and replacement with L-T3 showed that suppression of TSH required higher serum levels T3 in Mct8(-/y) than wild-type (WT) littermates, indicating hypothalamus and/or thyrotroph resistance to T3. Furthermore, T4 is required to maintain the high serum T3 level because the latter was not different between the two genotypes during administration of T3. Mct8(-/y) mice have 2.3-fold higher T3 content in liver associated with 6.1- and 3.1-fold increase in deiodinase 1 mRNA and enzymatic activity, respectively. The relative T3 excess in liver of Mct8(-/y) mice produced a decrease in serum cholesterol (79 +/- 18 vs. 137 +/- 38 mg/dl in WT) and an increase in alkaline phosphatase (107 +/- 23 vs. 58 +/- 3 U/liter in WT) levels. In contrast, T3 content in cerebrum was 1.8-fold lower in Mct8(-/y) mice, associated with a 1.6- and 10.6-fold increase in D2 mRNA and enzymatic activity, respectively, as previously observed in TH-deprived WT mice. We conclude that cell-specific differences in intracellular TH content due to differences in contribution of the various TH transporters are responsible for the unusual clinical presentation of this defect, in contrast to TH deficiency.

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Authors: Dumitrescu, A. M., Liao, X.-H., Weiss, R. E., Millen, K., & Refetoff, S.
Affiliations: University of Chicago (US)
Corresponding author: Refetoff, Samuel
ORCID: Dumitrescu, Alexandra M.
Weiss, Roy E.
Millen, Kathleen
Refetoff, Samuel
Venue: Endocrinology
Publisher: The Endocrine Society
Published: 2006-09-01
Volume: 147
Issue: 9
Pages: 4036-4043
ISSN: 0013-7227 (ISSN-L)
1945-7170
DOI: 10.1210/en.2006-0390
OpenAlex: W2102611661
Cited by: 318
References: 30
Citations by year: 2026: 4 · 2025: 7 · 2024: 7 · 2023: 3 · 2022: 19 · 2021: 15 · 2020: 11 · 2019: 20 · 2018: 9 · 2017: 21 · 2016: 18 · 2015: 24 · 2014: 23 · 2013: 19 · 2012: 17
FWCI: 13.53
Type: journal article
Language: en
Open access: closed
Locations: Endocrinology (publishedVersion)
PubMed (publishedVersion)
Funders: University of Chicago
National Institutes of Health (DK 15070)
National Institute of Diabetes and Digestive and Kidney Diseases (DK 15070, DK 58281, DK 20595, R01DK058281)
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: MCT8, thyroid hormone excess, deiodinase 2, T3, thyroxine, reverse T3, TSH suppression, liver, cerebrum, serum cholesterol, alkaline phosphatase, knockout mice
MeSH terms: Alkaline Phosphatase, Animals, Brain Chemistry, Cholesterol, Disease Models, Animal, Drug Resistance, Female, Humans, Hypothalamus, Kinetics, Liver, Male, Mice, Inbred C57BL, Mutation, Phenotype, Thyroid Hormones, Thyrotropin, Thyroxine, Triiodothyronine, Mice, Knockout, Membrane Transport Proteins, Monocarboxylic Acid Transporters, Symporters, Mice

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Tissue-Specific Thyroid Hormone Deprivation and Excess in Monocarboxylate Transporter (Mct) 8-Deficient Mice

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