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The sodium iodide symporter and thyroid disease
Author(s) -
Smyth Peter P. A.,
Dwyer Roisin M.
Publication year - 2002
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.2002.01474.x
Subject(s) - medicine , sodium iodide symporter , citation , endocrine system , library science , symporter , computer science , chemistry , hormone , biochemistry , transporter , gene
The movement of a variety of species from the iodine-rich environment of the sea to the relatively iodine-deficient land has necessitated the development of mechanisms which will trap more efficiently inorganic iodide (I – ) necessary for the formation of thyroid hormones (Venturi et al. , 2000). In man as in other mammals iodide uptake by the thyroid is mediated via a TSHdependent transmembrane protein, the sodium iodide symporter (NIS), so-called because it co-transports Na + with I – into the thyroid against the concentration gradient (De La Vieja et al. , 2000). The NIS is located in the basolateral membrane of thyroid follicular cells, and accumulated I – is organified to molecular iodine (I 2 ) through the action of the enzyme thyroid peroxidase (TPO) in the presence of H 2 O 2 , which takes place mainly at the apical membrane of the follicular cell. Organified iodine iodinates the thyroid protein thyroglobulin, which when stored in the lumen of thyroid follicles represents a storage site for the hormones thyroxine (T4) and triiodothyronine (T3) (Taurog, 1996). Possession of NIS enables the thyroid to concentrate I –