Department of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Biol Trace Elem Res. 2012 Jun;147(1-3):233-9. doi: 10.1007/s12011-011-9300-x. Epub 2012 Jan 6.
The aim of this study was to illustrate the combined effect of excess iodine and high-fat diet on lipid metabolism and its potential molecular mechanism. Sixty Balb/c mice were randomly allocated to three control groups or three excess iodine groups and fed with a high-fat diet in the absence or presence of 1,200 μg/L iodine for 1, 3, or 6 months, respectively. Serum lipid parameters and serum thyroid hormones were measured. Expressions of scavenger receptor class B type-I (SR-BI) and low density lipoproteins receptor (LDLr) mRNA and protein in liver were detected. Thyroid histology and liver type 1 iodothyronine deiodinase activity were analyzed. At the end of 3 and 6 months, compared with control, serum TC, TG, and LDL-C in excess iodine group were significantly lower (p < 0.05). LDLr expression in liver was increased significantly (p < 0.05) and parallel to the change of serum TC and TG. TT3 and TT4 levels in serum were elevated and TSH decreased significantly (p < 0.05). Liver type I iodothyronine deiodinase activity was significantly higher (p < 0.05) than control at the end of 6 months. Moreover, a time course damage effect of excess iodine combined with high-fat diet on thyroid glands was observed. The present findings demonstrated that excess iodine combined with high-fat diet could cause damage to thyroid glands and lead to thyroid hormone disorder. Those in turn caused the upregulation of hepatic LDLr gene, which resulted in the disorder in serum lipids.
本研究旨在阐明碘过量和高脂饮食对脂代谢的联合影响及其潜在的分子机制。将 60 只 Balb/c 小鼠随机分为三组对照或三组碘过量组，分别给予不含或含 1200μg/L 碘的高脂饮食 1、3 或 6 个月。检测血清脂质参数和血清甲状腺激素。检测肝脏中清道夫受体 B 型 1（SR-BI）和低密度脂蛋白受体（LDLr）mRNA 和蛋白的表达。分析甲状腺组织学和肝脏 1 型碘甲状腺原氨酸脱碘酶活性。在 3 个月和 6 个月结束时，与对照组相比，碘过量组的血清 TC、TG 和 LDL-C 显著降低（p < 0.05）。肝内 LDLr 表达明显增加（p < 0.05），与血清 TC 和 TG 的变化平行。血清 TT3 和 TT4 水平升高，TSH 显著降低（p < 0.05）。6 个月结束时，肝脏 1 型碘甲状腺原氨酸脱碘酶活性明显高于对照组（p < 0.05）。此外，还观察到碘过量与高脂饮食联合对甲状腺的时间进程损伤作用。本研究结果表明，碘过量与高脂饮食结合可导致甲状腺损伤，引起甲状腺激素紊乱。进而导致肝内 LDLr 基因上调，导致血清脂质紊乱。
