The expression of the sodium/iodide symporter is up-regulated in the thyroid of fetuses of iodine-deficient rats

Is the fetal thyroid already capable to increase its iodide uptake in respo nse to iodine deficiency? To answer this question, we analyzed the expressi on of the Na+/I- symporter and several other genes in the thyroid of rat fe tuses at 21 d of gestation from control mothers presenting a mild or more s evere 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 injectio n of 10 mu Ci Na I-125 into the dams. The absolute iodide uptake of the mat ernal thyroid was unchanged in a low iodine diet, not supplemented, compare d with one supplemented with iodide. In contrast, the fetal thyroid absolut e iodide uptake of a low iodine diet, not supplemented, and one supplemente d with perchlorate was decreased by 70% and 95% compared with that suppleme nted with iodide. Na+/I- symporter mRNA was detected in the fetal thyroid o f supplemented with iodide and increased about 2- and 4- fold in the thyroi d 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 thy roglobulin and type I deiodinase mRNA contents were only significantly incr eased with a diet supplemented with perchlorate. Glucose transporter 4 mRNA was decreased in the fetal thyroid of both a low iodine diet, not suppleme nted, 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 sh ow that all adaptive and/or defending mechanisms against iodine deficiency are already present in the fetus.