Severe iodine deficiency is characterized by goiter, preferential synthesis, and secretion of T(3) in thyroids, hypothyroxinemia in plasma and tissues, normal or low plasma T(3), and slightly increased plasma TSH. We studied changes in deiodinase activities and mRNA in several tissues of rats maintained on low-iodine diets (LIDs) or LIDs supplemented with iodine (LID+I). T(4) and T(3) concentrations decreased in plasma, tissues, and thyroids of LID rats, and T(4) decreased more than T(3) (50%). The highest type 1 iodothyronine deiodinase (D1) activities were found in the thyroid, kidney, and the liver; pituitary, lung, and ovary had lower D1 activities; but the lowest levels were found in the heart and skeletal muscle. D1 activity decreased in all tissues of LID rats (10-40% of LID+I rats), except for ovary and thyroids, which D1 activity increased 2.5-fold. Maximal type 2 iodothyronine deiodinase (D2) activities were found in thyroid, brown adipose tissue, and pituitary, increasing 6.5-fold in thyroids of LID rats and about 20-fold in the whole gland. D2 always increased in response to LID, and maximal increases were found in the cerebral cortex (19-fold), thyroid, brown adipose tissue, and pituitary (6-fold). Lower D2 activities were found in the ovary, heart, and adrenal gland, which increased in LID. Type 3 iodothyronine deiodinase activity was undetectable. Thyroidal Dio1 and Dio2 mRNA increased in the LID rats, and Dio1 decreased in the lung, with no changes in mRNA expression in other tissues. Our data indicate that LID induces changes in deiodinase activities, especially in the thyroid, to counteract the low T(4) synthesis and secretion, contributing to maintain the local T(3) concentrations in the tissues with D2 activity.

译文

:严重的碘缺乏症的特征是甲状腺肿大,甲状腺的优先合成和分泌T(3),血浆和组织中的甲状腺素低血症,血浆T(3)正常或较低以及血浆TSH略有增加。我们研究了低碘饮食(LIDs)或补充碘的LID(LID I)维持的大鼠几个组织中脱碘酶活性和mRNA的变化。在LID大鼠的血浆,组织和甲状腺中,T(4)和T(3)的浓度降低,而T(4)的降低幅度大于T(3)(50%)。在甲状腺,肾脏和肝脏中发现最高的1型碘甲状腺素脱碘酶(D1)活性。垂体,肺和卵巢的D1活性较低;但是最低的水平是在心脏和骨骼肌中发现的。除卵巢和甲状腺外,LID大鼠所有组织中的D1活性均降低(LID I大鼠的10-40%),D1活性提高了2.5倍。在甲状腺,褐色脂肪组织和垂体中发现最大的2型碘甲状腺素脱碘酶(D2)活性,在LID大鼠的甲状腺中增加了6.5倍,在整个腺体中增加了约20倍。 D2总是响应LID而增加,在大脑皮层(19倍),甲状腺,褐色脂肪组织和垂体(6倍)中发现最大的增加。在卵巢,心脏和肾上腺中发现较低的D2活性,而LID升高。无法检测到3型碘甲状腺素脱碘酶活性。 LID大鼠的甲状腺Dio1和Dio2 mRNA增加,而肺中Dio1减少,其他组织的mRNA表达没有变化。我们的数据表明,LID诱导脱碘酶活性的变化,尤其是在甲状腺中,以抵消低T(4)的合成和分泌,从而有助于维持具有D2活性的组织中的局部T(3)浓度。

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