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碘缺乏雌性大鼠甲状腺和组织中的脱碘酶活性。

Deiodinase activities in thyroids and tissues of iodine-deficient female rats.

机构信息

Instituto Investigaciones Biomédicas, Arturo Duperier, 4, 28029 Madrid, Spain.

出版信息

Endocrinology. 2013 Jan;154(1):529-36. doi: 10.1210/en.2012-1727. Epub 2012 Nov 9.

Abstract

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.

摘要

严重碘缺乏的特征是甲状腺肿大、优先合成和分泌 T3、血浆和组织中的甲状腺素血症、正常或低血浆 T3 和稍高的血浆 TSH。我们研究了在低碘饮食(LID)或 LID 补充碘(LID+I)的大鼠的几种组织中脱碘酶活性和 mRNA 的变化。LID 大鼠的血浆、组织和甲状腺中的 T4 和 T3 浓度降低,且 T4 降低的幅度大于 T3(50%)。I 型甲状腺素脱碘酶(D1)的最高活性见于甲状腺、肾脏和肝脏;垂体、肺和卵巢的 D1 活性较低;但心脏和骨骼肌的活性最低。除了卵巢和甲状腺,LID 大鼠的所有组织中的 D1 活性均降低(为 LID+I 大鼠的 10-40%),D1 活性增加了 2.5 倍。II 型甲状腺素脱碘酶(D2)的最大活性见于甲状腺、棕色脂肪组织和垂体,LID 大鼠甲状腺中的 D2 活性增加了 6.5 倍,整个腺体增加了约 20 倍。D2 总是对 LID 作出反应而增加,大脑皮层的增加幅度最大(19 倍),甲状腺、棕色脂肪组织和垂体(6 倍)。卵巢、心脏和肾上腺中的 D2 活性较低,在 LID 中增加。III 型甲状腺素脱碘酶活性无法检测。LID 大鼠的甲状腺 Dio1 和 Dio2 mRNA 增加,肺中的 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,以对抗低 T4 的合成和分泌,有助于维持具有 D2 活性的组织中的局部 T3 浓度。

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