临床研究发现，甲状腺功能减退症往往合并高胆固醇血症，而甲状腺功能亢进症则经常伴有血胆固醇水平的降低。因此，甲状腺功能异常疾病可以作为研究胆固醇代谢的特殊模型。近年来microRNA（miRNA）在脂代谢中的作用备受重视。为寻找新的参与胆固醇代谢的miRNA，我们比较了甲状腺功能正常、亢进和减退患者的血清miRNA表达谱，发现miR-10a/10b的表达差异显著。后续研究发现，甲状腺激素能够上调肝细胞中miR-10a/10b的表达。生物信息学分析提示， miR-10a/10b可能调控胆固醇合成代谢的重要因子——胰岛素诱导基因2(Insig2)。 本研究拟通过进一步的细胞实验和动物实验，阐明甲状腺激素调控miR-10a/10b表达的分子机制以及miR-10a/10b通过调控Insig2进而参与肝脏胆固醇代谢的具体通路，从而为脂代谢紊乱相关疾病的治疗寻找新的作用靶点。

Clinical studies have revealed that hypothyroidism is usually accompanied by hypercholesterolemia, while hyperthyroidism is frequently associated with reduced cholesterol levels. Therefore, thyroid dysfunction serves as an ideal and unique model to study cholesterol metabolism. Recently, evidence is mounting on microRNAs’ role in lipid metabolism. In an effort to identify microRNAs involved in cholesterol metabolism, we analyzed the serum microRNA profiles of euthyroid, hyper and hypo-thyroid patients. MicroRNA 10a/10b were shown to change significantly among them. T3 was confirmed to up-regulate the expression of microRNA 10a/10b in Hep3B cell line. Further bioinformatics analysis revealed that Insig2—an important regulator of cholesterol metabolism, is a target of microRNA 10a/10b. Next, we will study the molecular mechanism how microRNA 10a/10b is regulated by T3, and how hepatic cholesterol metabolism is influenced by microRNA 10a/10b and Insig2, so as to seek new targets for treating dyslipidemia.