Obregón M J, Ruiz de Oña C, Calvo R, Escobar del Rey F, Morreale de Escobar G
Unidad de Endocrinología Molecular, Universidad Autónoma de Madrid, Spain.
Endocrinology. 1991 Nov;129(5):2663-73. doi: 10.1210/endo-129-5-2663.
Female rats were fed a low iodine diet (LID) or the same diet supplemented with KI (IOD) and mated. Plasma TSH, T4 and T3 in thyroid, plasma, and tissues, and 5'-deiodinase activities (5'D) were measured in maternal, fetal, and neonatal samples. Plasma T4 was markedly reduced in LID dams, TSH was increased, and T3 was normal. Placental T4 was decreased to 10%, and placental T3 to 50%. In LID fetuses there was a complete depletion of both extrathyroidal and intrathyroidal stores of T4 and T3. The thyroid responded with increased synthesis and secretion of T3 over T4, as assessed from the T3 to T4 ratios. Near birth, brain T4 and T3 concentrations were only 6.7% and 12% of those in IOD fetuses, despite a marked increase in brain 5'D-II and a T4-sparing decrease in liver and lung 5'D-I. Brown adipose tissue 5'D-II increased 7-fold, and brown adipose tissue T4 and T3 concentrations were only decreased by 50%. After birth, the availability of iodine improved somewhat through maternal milk, and the thyroidal and extrathyroidal pools of T4 and T3 increased, although they remained much lower than those in IOD pups. Brain 5'D-II markedly increased in LID pups, and this together with an increase in plasma and brain T4 ensured almost normal brain T3 during the suckling period. The thyroidal secretion of T3 over T4 continued to be increased in LID pups during the suckling period and appeared to be related to their high circulating TSH levels. Both LID fetuses and newborns can respond to iodine deficiency as adults rats, but the fetus is more sensitive to LID because of its dependence on maternal T4. The success of the adaptative mechanisms in protecting the brain from severe T3 deficiency depends on the supply of iodine, the limiting factor for the synthesis of T4.
将雌性大鼠分为两组，一组喂食低碘饮食（LID），另一组喂食添加碘化钾（IOD）的相同饮食，然后使其交配。分别检测母体、胎儿和新生儿样本中的血浆促甲状腺激素（TSH）、甲状腺、血浆及组织中的甲状腺素（T4）和三碘甲状腺原氨酸（T3），以及5'-脱碘酶活性（5'D）。LID组母鼠血浆T4显著降低，TSH升高，T3正常。胎盘T4降至10%，胎盘T3降至50%。LID组胎儿甲状腺外和甲状腺内的T4和T3储备完全耗尽。从T3与T4的比值评估，甲状腺对T3的合成和分泌增加，超过了T4。临近出生时，尽管脑5'D-II显著增加，肝脏和肺5'D-I减少以节省T4，但脑T4和T3浓度仅为IOD组胎儿的6.7%和12%。棕色脂肪组织5'D-II增加7倍，棕色脂肪组织T4和T3浓度仅降低50%。出生后，通过母乳碘供应有所改善，甲状腺及甲状腺外的T4和T3储备增加，尽管仍远低于IOD组幼崽。LID组幼崽脑5'D-II显著增加，加上血浆和脑T4增加，确保了哺乳期脑T3几乎正常。哺乳期LID组幼崽甲状腺T3与T4的分泌持续增加，这似乎与它们循环中高TSH水平有关。LID组胎儿和新生儿都能像成年大鼠一样对碘缺乏做出反应，但胎儿对LID更敏感，因为其依赖母体T4。适应性机制成功保护大脑免受严重T3缺乏的影响取决于碘的供应，碘是合成T4的限制因素。
