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

严重缺碘的特征是甲状腺肿大,甲状腺优先合成和分泌T(3),血浆和组织中的低甲状腺素血症,正常或低血浆T(3) 和血浆TSH略有升高。我们研究了低碘饮食 (LID) 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。LID大鼠血浆,组织和甲状腺中T(4) 和T(3) 的浓度降低,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型碘甲状腺原氨酸脱碘酶 (D1) 活性; 垂体,肺和卵巢的D1活性较低; 但在心脏和骨骼肌中发现最低水平。除卵巢和甲状腺外,LID大鼠的所有组织 (LID I大鼠的10-40%) 中的D1活性均降低,D1活性增加了2.5倍。在甲状腺,棕色脂肪组织和垂体中发现最大的2型碘甲状腺原氨酸脱碘酶 (D2) 活性,在LID大鼠的甲状腺中增加6.5倍,在整个腺体中约增加20倍。D2总是响应LID而增加,并且在大脑皮层 (19倍),甲状腺,棕色脂肪组织和垂体 (6倍) 中发现最大增加。在卵巢,心脏和肾上腺中发现较低的D2活性,在LID中增加。无法检测到3型碘甲状腺原氨酸脱碘酶活性。LID大鼠甲状腺Dio1和Dio2 mRNA增加,肺中Dio1降低,其他组织中mRNA表达无变化。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,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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