中国病理生理杂志2016，Vol.32Issue(4)：738-744,7.DOI:10.3969/j.issn.1000-4718.2016.04.026
胰岛素抵抗小鼠血清微小RNA的芯片及信息学分析
Chip and informatic analysis of serum microRNA levels in insulin-resis-tant mice
摘要
Abstract
AIM:To study the microRNA profiling in the serum of insulin-resistant mice and the mechanism of insulin resistance induced by related microRNAs.METHODS:A high-fat diet was used to induce insulin resistance model in KM mice.The microRNA profiling in serum of insulin-resistant and normal mice was analyzed by microarray chip and were validated by real-time PCR.miRanda data base was used to forecast target genes.miRBase was used to obtain the se-quences of related microRNAs, based on which protein interactions were predicted using the online analytical tool STRING. RESULTS:In serum of insulin-resistant mice, the expression of miR-125, miR-126, miR-143, miR-30a, miR-199a, miR-127, miR-184, miR-30e, miR-134, miR-195, miR-206, miR-429, miR-212, miR-362, miR-382, miR-154 and miR-466h was significantly up-regulated.miR-211, miR-504, miR-877 and miR-1930 were significantly down-regulated. miR-143 associated with insulin resistance was able to bind to 3'-UTR of fat mass and obesity-associated protein (FTO), and FTO was found to interact with Rpgrip1l, Tmem18, Mc4r, Npy, Hhex, Tcf712, Cdkal1, Slc30a8, Igf2bp2 and Tha-da.CONCLUSION:Twenty-one microRNAs in the serum of insulin-resistant mice induced by a high-fat diet are signifi-cantly different from those of normal mice, in which 17 kinds were significantly up-regulated.miR-143 closely related to in-sulin resistance is able to regulate FTO protein expression, which interacts with other 10 proteins associated with the occur-rence and development of diabetes.The results are also useful for further study of the molecular mechanisms in insulin re-sistance.关键词
胰岛素抵抗/微小RNA/芯片/信息学Key words
Insulin resistance/MicroRNAs/Chip/Informatics分类
医药卫生引用本文复制引用
徐志伟,王文栋,常晓彤..胰岛素抵抗小鼠血清微小RNA的芯片及信息学分析[J].中国病理生理杂志,2016,32(4):738-744,7.基金项目
张家口市科技局项目(No.12110065G-5) （No.12110065G-5）
河北省教育厅项目(No.QN2016175) （No.QN2016175）
