Morreale de Escobar G, Obregón M J, Calvo R, Escobar del Rey F
Unidad de Endocrinología Molecular, Instituto de Investigaciones Biomédicas, Facultad de Medicina UAM, Madrid, Spain.
Am J Clin Nutr. 1993 Feb;57(2 Suppl):280S-285S. doi: 10.1093/ajcn/57.2.280S.
Thyroid hormones, thyroxin (T4) and 3,5,3'-triiodothyronine (T3), of maternal origin, are available to the mammalian embryo early in development. However, after the onset of fetal thyroid function, they are of both fetal and maternal origin. Maternal T4 has a protective effect on the fetal brain in cases of congenital hypothyroidism. In severe iodine deficiency, maternal T4 is low, although T3 is normal; the developing embryo is markedly T4-deficient; and T3 deficiency increases with gestational age. In contrast to mechanisms in the hypothyroid fetus from a normal mother, the low T4 of the iodine-deficient mother prevents any protective effects on the fetal brain. Thyroid hormone deficiency of the iodine-deficient fetus, including the brain, is more severe and prolonged than it is in the cases of maternal or fetal thyroid failures. These findings may help to explain the relationship between severe maternal hypothyroxinemia and the severe central nervous system damage of the neurological endemic cretin.
源自母体的甲状腺激素，即甲状腺素（T4）和3,5,3'-三碘甲腺原氨酸（T3），在哺乳动物胚胎发育早期即可获取。然而，在胎儿甲状腺功能开始发挥作用后，它们既来源于胎儿也来源于母体。在先天性甲状腺功能减退的情况下，母体T4对胎儿大脑具有保护作用。在严重碘缺乏时，母体T4水平较低，尽管T3正常；发育中的胚胎明显缺乏T4；并且T3缺乏随着胎龄增加而加重。与正常母亲所生的甲状腺功能减退胎儿的机制不同，碘缺乏母亲的低T4无法对胎儿大脑产生任何保护作用。碘缺乏胎儿的甲状腺激素缺乏，包括大脑，比母体或胎儿甲状腺功能衰竭的情况更为严重且持续时间更长。这些发现可能有助于解释严重母体甲状腺素血症与神经型地方性克汀病严重中枢神经系统损害之间的关系。
