CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Iodide regulates Na+/I- symporter expression in the kidney
Autor/es:
NICOLA, JP; SERRANO-NASCIMENTO, C; CALIL-SILVEIRA, J; NUNEZ, MT; MASINI-REPISO, AM
Lugar:
Lima
Reunión:
Congreso; XIV Congreso de la Sociedad Latinoamericana de Tiroides; 2011
Institución organizadora:
Sociedad Latinoamericana de Tiroides
Resumen:
Background. How the kidney regulates iodide excretion is
poorly understood. Iodide elimination occurs primarily through the
kidney, being excreted in urine as inorganic iodide. Iodide is freely filtered
at the glomerulus and partially reabsorbed along the tubular epithelium through
both passive and active mechanisms. However, the events involved in its tubular
recovery are poorly characterized.
Originally
identified in the thyroid, the Na+/I- symporter (NIS) is an integral plasma
membrane glycoprotein able to specifically mediate iodide transport in many
tissues, playing an important role in iodide metabolism. Interestingly, NIS expression was demonstrated in the renal tubular
system, suggesting that NIS
might be involved in renal iodide transport.
Objective. To investigate a role of NIS-mediated iodide
reabsorption, we examined the regulation of renal NIS expression by high plasma iodide
concentrations.
Methods. Male Wistar rats were subjected to iodide rich
diet (0.05% I--supplemented drinking water) for 1, 2 and 6 days in
the chronic experiments (n=8/group), or received a single 0.01, 0.1 or 1 mg ip
injection of iodide for 24 h in the acute model (n=4/group). Thereafter, total kidney
RNA extraction was performed and NIS
mRNA abundance was evaluated by real-time PCR.
Results. We observed a significant reduction of NIS mRNA abundance in
rats subjected to chronic iodide ingestion after 2 and 6 days. Similarly, in
the acute model, we measured a significant decrease of NIS mRNA expression at all the tested
concentrations of iodide.
Conclusions. High plasma iodide concentrations repressed
renal NIS mRNA
expression. Thus, these findings lead to propose a potential role of NIS in the renal
regulation of iodide excretion; in turn contributing to the maintenance of iodide
homeostasis.