Best Practice & Research Clinical Endocrinology & Metabolism
Volume 21, Issue 2 , Pages 223-236, June 2007

Thyroid hormone transport by monocarboxylate transporters

  • Theo J. Visser, PhD (Professor)

      Affiliations

    • Corresponding Author InformationCorresponding author. Tel.: +31 10 463 5463; Fax: +31 10 463 5430.

Department of Internal Medicine, Erasmus Medical Center, Dr Molewaterplein 50, 3015 GE Rotterdam, The Netherlands

Thyroid hormone (TH) is essential for the normal development and metabolism of different tissues. TH action and metabolism take place intracellularly, which requires cellular uptake via transporters. Several transporter families have been identified, of which the monocarboxylate transporter (MCT) family deserves special attention. So far, only MCT1, MCT2, MCT3, MCT4 and MCT6 have been demonstrated to transport monocarboxylates; MCT8 has been identified as a specific TH transporter. MCT8 mutations in humans are associated with severe psychomotor retardation and elevated 3,3′,5-triiodothyronine (T3) levels. Recently, MCT8 knockout mice have been shown to perfectly imitate the thyroid state in patients with MCT8 mutations; however, they lack the neurological defects. Although it was long hypothesized that a T-type amino acid transporter also transports iodothyronines, it only recently became clear that MCT10 is involved in the bidirectional transport of aromatic amino acids and iodothyronines. MCT10 preferentially transports T3 even more effectively than does MCT8. However, its precise function in the human body is poorly understood.

Key words: MCT, MCT8, MCT10, monocarboxylate transporter, TAT1, thyroid hormone transporter

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PII: S1521-690X(07)00030-9

doi:10.1016/j.beem.2007.03.008

Best Practice & Research Clinical Endocrinology & Metabolism
Volume 21, Issue 2 , Pages 223-236, June 2007