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The Expression of the Sodium/Iodide Symporter Is Up-Regulated in the Thyroid of Fetuses of Iodine-Deficient Rats

Unidad de Endocrinologia Molecular (J.P.S., M.J.O.), Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Cientificas, 28029 Madrid, Spain; Human and Animal Physiology (D.v.d.H., J.K.), Wageningen University, 6709 PJ Wageningen, The Netherlands; INSERM, Unité 369 (B.R.), Faculté de Médicine Lyon-RTH Laënnec, F69372 Lyon, France

Address all correspondence and requests for reprints to: Dr. J. P. Schröder-van der Elst, Human and Animal Physiology, Wageningen University, Haarweg 10, 6709 PJ Wageningen, The Netherlands. E-mail: Janny.vanderElst{at}alg.fmd.wau.nl

Is the fetal thyroid already capable to increase its iodide uptake in response to iodine deficiency? To answer this question, we analyzed the expression of the Na⁺/I^- symporter and several other genes in the thyroid of rat fetuses at 21 d of gestation from control mothers presenting a mild or more severe iodine deficiency. Female rats were placed on a low iodine diet, not supplemented, or supplemented with iodide or perchlorate for 3 months. The maternal and fetal thyroidal iodide uptake was measured 24 h after injection of 10 µCi Na ¹²⁵I into the dams. The absolute iodide uptake of the maternal thyroid was unchanged in a low iodine diet, not supplemented, compared with one supplemented with iodide. In contrast, the fetal thyroid absolute iodide uptake of a low iodine diet, not supplemented, and one supplemented with perchlorate was decreased by 70% and 95% compared with that supplemented with iodide. Na⁺/I^- symporter mRNA was detected in the fetal thyroid of supplemented with iodide and increased about 2- and 4- fold in the thyroid of fetuses from a low iodine diet, not supplemented, and one supplemented with perchlorate, respectively. Na⁺/I^- symporter expression was induced in the fetal side of the placenta in both a low iodine diet, not supplemented, and one supplemented with perchlorate; in contrast, Na⁺/I^- symporter mRNA was never detected in the maternal side of the placenta. Fetal thyroid thyroglobulin and type I deiodinase mRNA contents were only significantly increased with a diet supplemented with perchlorate. Glucose transporter 4 mRNA was decreased in the fetal thyroid of both a low iodine diet, not supplemented, and one supplemented with perchlorate compared with one supplemented with iodide.

In conclusion, although the up-regulation of Na⁺/I^- symporter expression in fetal thyroid and placenta in the low iodine diet, not supplemented group did not lead to restoration of a normal absolute iodide uptake, our data show that all adaptive and/or defending mechanisms against iodine deficiency are already present in the fetus.

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