Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
Institut für Experimentelle Endokrinologie, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, CVK, Berlin, Germany.
J Clin Endocrinol Metab. 2019 Feb 1;104(2):568-580. doi: 10.1210/jc.2018-01713.
To investigate the importance of dietary selenium (Se) for hyperthyroidism.
We performed a more in-depth analysis of a large cross-sectional study of 6152 participants from two counties within the Shaanxi Province, China. These counties are characterized by different habitual Se intake. We investigated the effects of a different dietary Se supply (0.02, 0.18, 0.6, or 2.0 ppm Se) on disease development in a mouse model of Graves disease (GD).
The cross-sectional study revealed a comparable prevalence of hyperthyroidism, irrespective of Se intake, in both counties. However, an unexpected sex-specific difference was noted, and Se deficiency might constitute a risk factor for hyperthyroidism, especially in males. In a mouse model, pathological thyroid morphology was affected, and greater Se intake exerted some protecting effects on the pathological distortion. Circulating thyroid hormone levels, malondialdehyde concentrations, total antioxidant capacity, and the titer of GD-causing TSH receptor autoantibodies were not affected by Se. Expression analysis of the transcripts in the spleen indicated regulatory effects on genes implicated in the immune response, erythropoiesis, and oxygen status. However, the humoral immune response, including the CD4/CD8 or T-helper 1/T-helper 2 cell ratio and the concentration of regulatory T cells, was similar between the experimental groups, despite the difference in Se intake.
Our data have highlighted a sexual dimorphism for the interaction of Se and thyroid disease risk in humans, with indications of a local protective effects of Se on thyroid gland integrity, which appears not to be reflected in the circulating biomarkers tested.
探讨膳食硒(Se)对甲状腺功能亢进症的重要性。
我们对来自中国陕西省两个县的 6152 名参与者进行了一项更深入的横断面研究。这些县的特点是习惯性硒摄入量不同。我们研究了不同膳食硒供应(0.02、0.18、0.6 或 2.0ppm Se)对格雷夫斯病(GD)小鼠模型中疾病发展的影响。
横断面研究显示,两个县的甲亢患病率相当,与硒摄入量无关。然而,令人意外的是,观察到了性别特异性差异,硒缺乏可能是甲亢的一个危险因素,尤其是在男性中。在小鼠模型中,甲状腺形态学发生了病理改变,而更多的硒摄入对病理扭曲有一定的保护作用。循环甲状腺激素水平、丙二醛浓度、总抗氧化能力和导致 GD 的 TSH 受体自身抗体滴度不受硒的影响。脾脏转录本的表达分析表明,硒对涉及免疫反应、红细胞生成和氧状态的基因具有调节作用。然而,尽管硒摄入量存在差异,但体液免疫反应,包括 CD4/CD8 或 T 辅助 1/T 辅助 2 细胞比值和调节性 T 细胞浓度,在实验组之间相似。
我们的数据强调了硒与人类甲状腺疾病风险相互作用的性别二态性,表明硒对甲状腺完整性具有局部保护作用,但这似乎没有反映在测试的循环生物标志物中。