Referenced in: none

Automatically associated channels: ClC4 , ClC5 , Slo1

Title: Thyroid iodide efflux: a team effort?

Authors: Peying Fong

Journal, date & volume: J. Physiol. (Lond.), 2011 Dec 15 , 589, 5929-39

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21986207

Abstract
The thyroid hormones thyroxine (T(4)) and triiodothyronine (T(3)) play key roles in regulating development, growth and metabolism in pre- and postnatal life. Iodide (I(-)) is an essential component of the thyroid hormones and is accumulated avidly by the thyroid gland. The rarity of elemental iodine and I(-) in the environment challenges the thyroid to orchestrate a remarkable series of transport processes that ultimately ensure sufficient levels for hormone synthesis. In addition to actively extracting circulating I(-), thyroid follicular epithelial cells must also translocate I(-) into a central intrafollicular compartment, where thyroglobulin is iodinated to form the protein precursor to T(4) and T(3). In the last decade, several bodies of evidence render questionable the notion that I(-) exits thyrocytes solely via the Cl(-)/I(-) exchanger Pendrin (SLC26A4), therefore necessitating reconsideration of several other candidate I(-) conduits: the Cl(-)/H(+) antiporter, CLC-5, the cystic fibrosis transmembrane conductance regulator (CFTR) and the sodium monocarboxylic acid transporter (SMCT1).