INTESTINAL NA+/I- SIMPORTER (NIS) EXPRESSION IS REGULATED AT POST-TRANSCIPTIONAL LEVEL BY HIGH CONCENTRATIONS OF IODIDE

NICOLA JP MASINI-REPISO AM.; SUSPERREGUY S; CARRASCO N; MASINI-REPISO AM.

Gramado, Brasil. Mayo 2009.

Congreso; XII Congreso de la Sociedad Latinoamericana de Tiroides (LATS); 2009

Iodide (I-) uptake in the thyroid gland is the first step in the biosynthesis of the thyroidhormones triiodothyronine (T3) and thyroxine (T4) of which iodine is an essential constituent(1). T3 and T4 are the only iodine-containing hormones in vertebrates and are required forthe development of the central nervous system and lungs in the fetus and newborn.Iodine is extremely scarce in the environment and is only supplied to the body through thediet. Insufficient dietary intake of iodine, depending on its severity, causes hypothyroidism,goiter, stunted growth, retarded psychomotor development, and irreversible mentalretardation (cretinism) (2).Active I- accumulation in the thyroid is mediated by the Na+/I- symporter (NIS), a plasmamembrane glycoprotein (1). The presence of NIS in the thyroid appears to be an adaptationto compensate for the environmental scarcity of iodine.Dietary iodide absorption in the gastrointestinal tract constitutes the first step in iodidemetabolism. Given the physiological significance of this halogen, the question of where andhow dietary I- is absorbed in the gastrointestinal tract has long been of major interest.We have recently described NIS expression and function on the apical surface of theintestinal epithelium as the central component of the iodide absorption system (3). However,the mechanisms involved in intestinal NIS regulation have not been disclosed.