Open AccessMonocarboxylate transporter 8 deficiency: altered thyroid morphology and persistent high triiodothyronine/thyroxine ratio after thyroidectomy
Author(s) -
Eva K. Wirth,
SienYi Sheu,
Jazmin Chiu-Ugalde,
Rémy Sapin,
Marc Klein,
Ilona Moßbrugger,
Leticia QuintanillaMartinez,
Martin Hrabě de Angelis,
Heiko Krude,
T Riebel,
K Rothe,
Josef Köhrle,
Kurt Werner Schmid,
Ulrich Schweizer,
Annette Grüters
Publication year - 2011
Publication title -
european journal of endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 148
eISSN - 1479-683X
pISSN - 0804-4643
DOI - 10.1530/eje-11-0369
Subject(s) - endocrinology , thyroidectomy , medicine , thyroid , levothyroxine , triiodothyronine , hormone , thyroid carcinoma
Thyroid hormone transport across the plasma membrane depends on transmembrane transport proteins, including monocarboxylate transporter 8 (MCT8). Mutations in MCT8 (or SLC16A2) lead to a severe form of X-linked psychomotor retardation, which is characterised by elevated plasma triiodothyronine (T(3)) and low/normal thyroxine (T(4)). MCT8 contributes to hormone release from the thyroid gland.
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