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孕期和哺乳期碘过量暴露会损害大鼠的母体甲状腺功能。

Iodine excess exposure during pregnancy and lactation impairs maternal thyroid function in rats.

作者信息

Serrano-Nascimento Caroline, Salgueiro Rafael Barrera, Vitzel Kaio Fernando, Pantaleão Thiago, Corrêa da Costa Vânia Maria, Nunes Maria Tereza

机构信息

Department of Physiology and BiophysicsInstitute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

Department of Physiology and BiophysicsInstitute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.

出版信息

Endocr Connect. 2017 Oct;6(7):510-521. doi: 10.1530/EC-17-0106. Epub 2017 Aug 16.

DOI:10.1530/EC-17-0106
PMID:28814477
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5597975/
Abstract

Adequate maternal iodine consumption during pregnancy and lactation guarantees normal thyroid hormones (TH) production, which is crucial to the development of the fetus. Indeed, iodine deficiency is clearly related to maternal hypothyroidism and deleterious effects in the fetal development. Conversely, the effects of iodine excess (IE) consumption on maternal thyroid function are still controversial. Therefore, this study aimed to investigate the impact of IE exposure during pregnancy and lactation periods on maternal hypothalamus-pituitary-thyroid axis. IE-exposed dams presented reduced serum TH concentration and increased serum thyrotropin (TSH) levels. Moreover, maternal IE exposure increased the hypothalamic expression of and the pituitary expression of and mRNA, while reduced the mRNA content. Additionally, IE-exposed dams presented thyroid morphological alterations, increased thyroid oxidative stress and decreased expression of thyroid genes/proteins involved in TH synthesis, secretion and metabolism. Furthermore, mRNA expression and D1 activity were reduced in the liver and the kidney of IE-treated animals. Finally, the mRNA expression of and were reduced in the mammary gland of IE-exposed rats. The latter results are in accordance with the reduction of prolactin expression and serum levels in IE-treated dams. In summary, our study indicates that the exposure to IE during pregnancy and lactation induces primary hypothyroidism in rat dams and impairs iodide transfer to the milk.

摘要

孕期和哺乳期母体摄入充足的碘可保证甲状腺激素(TH)正常分泌,这对胎儿发育至关重要。事实上,碘缺乏与母体甲状腺功能减退及胎儿发育的有害影响明显相关。相反,过量碘(IE)摄入对母体甲状腺功能的影响仍存在争议。因此,本研究旨在探讨孕期和哺乳期暴露于IE对母体下丘脑-垂体-甲状腺轴的影响。暴露于IE的母鼠血清TH浓度降低,血清促甲状腺激素(TSH)水平升高。此外,母体暴露于IE会增加下丘脑 的表达以及垂体 和 mRNA的表达,同时降低 mRNA含量。此外,暴露于IE的母鼠出现甲状腺形态改变、甲状腺氧化应激增加,以及参与TH合成、分泌和代谢的甲状腺基因/蛋白质表达降低。此外,IE处理动物的肝脏和肾脏中 mRNA表达和D1活性降低。最后,暴露于IE的大鼠乳腺中 和 的mRNA表达降低。后一结果与IE处理母鼠中催乳素表达和血清水平降低一致。总之,我们的研究表明,孕期和哺乳期暴露于IE会导致母鼠原发性甲状腺功能减退,并损害碘向乳汁中的转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb47/5597975/9b2c1de5ac6a/ec-6-510-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb47/5597975/496466a36481/ec-6-510-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb47/5597975/37a719e04c73/ec-6-510-g002.jpg
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