Maternal selenium deficiency during pregnancy in mice increases thyroid hormone concentrations, alters placental function and reduces fetal growth
Maternal selenium deficiency during pregnancy in mice increases thyroid hormone concentrations, alters placental function and reduces fetal growth
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DOI：
10.1113/jp278473
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发表时间：
2019-10-30
影响因子：
5.5
通讯作者：
Cuffe, James S. M.
中科院分区：
文献类型：
--
作者：
Hofstee, Pierre;Bartho, Lucy A.;Cuffe, James S. M.
关键点妊娠期关键微量营养素摄入不当会改变母体内分泌状态，损害胎盘发育并诱导胎儿生长受限。硒是一种必需的微量营养素，约25种重要蛋白质的功能所需。然而，妊娠期硒缺乏对母体、胎盘和胎儿结局的具体影响知之甚少。目前的研究表明，母亲硒缺乏增加母体三碘甲状腺原氨酸和四碘甲状腺原氨酸浓度，降低胎儿血糖浓度，并诱导胎儿生长受限。关键的硒依赖性甲状腺激素转换酶的胎盘表达减少，而关键的胎盘营养转运蛋白的表达失调。硒缺乏对硒依赖性抗氧化剂的影响最小，但增加胎盘铜浓度和超氧化物歧化酶1的表达。这些结果强调了这样一种观点，即妊娠期间硒缺乏可能导致甲状腺功能障碍，导致胎儿生长减少，这可能先于后代的程序性疾病结果。硒是一种微量元素，对各种体内平衡过程至关重要，包括抗氧化调节和甲状腺激素代谢。妊娠期缺硒很常见，会增加妊娠并发症的风险，包括胎儿生长受限。虽然胎盘形成的改变可能导致这些不良结局，但硒缺乏导致妊娠并发症的机制尚不清楚。雌性C57 BL/6小鼠随机分为对照组（>190 μ g kg（-1），n = 8）和低硒组（
Key pointsInappropriate intake of key micronutrients in pregnancy is known to alter maternal endocrine status, impair placental development and induce fetal growth restriction. Selenium is an essential micronutrient required for the function of approximately 25 important proteins. However, the specific effects of selenium deficiency during pregnancy on maternal, placental and fetal outcomes are poorly understood. The present study demonstrates that maternal selenium deficiency increases maternal triiodothyronine and tetraiodothyronine concentrations, reduces fetal blood glucose concentrations, and induces fetal growth restriction. Placental expression of key selenium-dependent thyroid hormone converting enzymes were reduced, whereas the expression of key placental nutrient transporters was dysregulated. Selenium deficiency had minimal impact on selenium-dependent anti-oxidants but increased placental copper concentrations and expression of superoxide dismutase 1. These results highlight the idea that selenium deficiency during pregnancy may contribute to thyroid dysfunction, causing reduced fetal growth, that may precede programmed disease outcomes in offspring. Selenium is a trace element fundamental to diverse homeostatic processes, including anti-oxidant regulation and thyroid hormone metabolism. Selenium deficiency in pregnancy is common and increases the risk of pregnancy complications including fetal growth restriction. Although altered placental formation may contribute to these poor outcomes, the mechanism by which selenium deficiency contributes to complications in pregnancy is poorly understood. Female C57BL/6 mice were randomly allocated to control (>190 mu g kg(-1), n = 8) or low selenium (