Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.
Biol Trace Elem Res. 2013 Jul;154(1):103-10. doi: 10.1007/s12011-013-9705-9. Epub 2013 May 28.
Iodine excess is emerging as a new focus. A better understanding of its hazardous effects on the liver will be of great benefit to health. The aim of this study is to illustrate the effects of iodine excess on hepatic lipid homeostasis and explore its possible mechanisms. One hundred twenty BaLB/c mice were given iodine at different levels (0, 0.3, 0.6, 1.2, 2.4, and 4.8 mg I/L) in drinking water for 1 or 3 months. Lipid parameters and serum thyroid hormones were measured. Hepatic type 1 deiodinase activity and oxidative stress parameters were evaluated. The mRNA expression of sterol regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) was detected by real-time polymerase chain reaction. Dose-dependent increase of hepatic triglyceride content was detected (r = 0.680, P < 0.01) in iodine-loaded groups. Evident hepatic steatosis was observed in 2.4 and 4.8 mg I/L iodine-loaded groups. The activities of antioxidant enzymes (glutathione peroxidase and superoxide dismutase) were decreased, and the malondialdehyde level was increased by excessive iodine in both serum and liver in a dose-dependent manner, accompanying the decrease of hepatic D1 activity. That resulted in the increase of serum total thyroxine and the decrease of serum total triiodothyronine in iodine-loaded groups. The mRNA expression of SREBP-1c and FAS was increased in iodine-loaded groups in response to the change of serum triiodothyronine. Present findings demonstrated that iodine excess could dose dependently induce hepatic steatosis. Furthermore, our data suggested that the disturbance of thyroid hormone metabolism involving oxidative stress may play a critical role in iodine excess-induced hepatic steatosis.
碘过量正成为一个新的关注点。更好地了解碘过量对肝脏的危害作用将对健康大有裨益。本研究旨在阐明碘过量对肝脂稳态的影响，并探讨其可能的机制。将 120 只 BaLB/c 小鼠分别给予不同水平（0、0.3、0.6、1.2、2.4 和 4.8 mg I/L）的碘饮水 1 或 3 个月。检测脂质参数和血清甲状腺激素。评估肝 1 型脱碘酶活性和氧化应激参数。实时聚合酶链反应检测固醇调节元件结合蛋白-1c（SREBP-1c）和脂肪酸合酶（FAS）的 mRNA 表达。在碘负荷组中检测到肝三酰甘油含量呈剂量依赖性增加（r=0.680，P<0.01）。在 2.4 和 4.8 mg I/L 碘负荷组中观察到明显的肝脂肪变性。抗氧化酶（谷胱甘肽过氧化物酶和超氧化物歧化酶）的活性降低，丙二醛水平升高，且随着肝 D1 活性的降低，血清和肝脏中均呈剂量依赖性，导致血清总甲状腺素增加，总三碘甲状腺原氨酸降低。在碘负荷组中，SREBP-1c 和 FAS 的 mRNA 表达增加，以响应血清三碘甲状腺原氨酸的变化。本研究结果表明，碘过量可剂量依赖性地诱导肝脂肪变性。此外，我们的数据表明，涉及氧化应激的甲状腺激素代谢紊乱可能在碘过量诱导的肝脂肪变性中起关键作用。
