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 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 microCi Na (125)I 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.
Schröder-van der Elst
J P
JP
Unidad de Endocrinologia Molecular, Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Cientificas, 28029 Madrid, Spain. Janny.vanderElst@alg.fmd.wau.nl
van der Heide
D
D
Kastelijn
J
J
Rousset
B
B
Obregón
M J
MJ
D000818:Animals; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D004032:Diet; D005260:Female; D005333:Fetus / Q000378:metabolism; D007455:Iodine / Q000008:administration & dosage / Q000172:deficiency* / Q000493:pharmacokinetics; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D010920:Placenta / Q000378:metabolism; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism*; D011270:Pregnancy, Animal / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D027981:Symporters; D013961:Thyroid Gland / Q000196:embryology*; D014018:Tissue Distribution; D015854:Up-Regulation; D000099209:Sodium-Iodide Symporters
D002352:Carrier Proteins; D007455:Iodine; D008565:Membrane Proteins; D012333:RNA, Messenger; D027981:Symporters; D000099209:Sodium-Iodide Symporters