Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter.

NICOLA, JP; REYNA-NEYRA, A; CARRASCO, N; MASINI-REPISO, AM

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2012 vol. 590 p. 6013 - 6013

1469-7793

ietary I(-) absorption in the gastrointestinal tract is the first step in I(-) metabolism. Given that I(-) is an essential constituent of the thyroid hormones, its concentrating mechanism is of significant physiological importance. We recently described the expression of the Na(+)/I(-) symporter (NIS) on the apical surface of the intestinal epithelium as a central component of the I(-) absorption system and reported reduced intestinal NIS expression in response to an I(-)-rich diet in vivo. Here, we evaluated the mechanism involved in the regulation of NIS expression by I(-) itself in enterocytes. Excess I(-) reduced NIS-mediated I(-) uptake in IEC-6 cells in a dose- and time-dependent fashion, which was correlated with a reduction of NIS expression at the plasma membrane. Perchlorate, a competitive inhibitor of NIS, prevented these effects, indicating that an increase in intracellular I(-) regulates NIS. Iodide induced rapid intracellular recruitment of pl