miR-23a/b-3p promotes hepatic lipid accumulation by regulating Srebp-1c and Fas
miR-23a/b-3p promotes hepatic lipid accumulation by regulating Srebp-1c and Fas
复制标题
miR-23a/b-3p通过调节Srebp-1c和Fas促进肝脏脂质积累
DOI：
10.1530/jme-20-0324
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发表时间：
2022-01-01
影响因子：
3.5
通讯作者：
Li, Jian
中科院分区：
文献类型：
--
作者：
Li, Linfang;Zhang, Xiaoyi;Li, Jian
miR-23a-3p和miR-23b-3p是miR-23 similar to 27 similar to 24 similar to 2超家族的成员。miR-23 a/B-3 p在调节肝脏脂质蓄积中的作用仍不清楚。在这里，我们发现miR-23 a-3p和miR-23 b-3p水平的增加伴随着高脂饮食小鼠和瘦素受体缺陷型2型糖尿病小鼠脂肪变性肝脏中固醇调节元件结合蛋白-1（SREBP-1）和脂肪酸合成酶（FAS）蛋白水平的增加（db/db）。miR-23 a/B-3p在Hep1 - 6细胞中的过表达可升高细胞内甘油三酯水平，并上调Srebp-1c和Fas的表达。综上所述，这些结果表明miR-23 a/B-3p通过结合Srebp-1c和Fas mRNA的5'-UTR增强mRNA稳定性，从而促进肝细胞中甘油三酯的积累。
miR-23a-3p and miR-23b-3p are members of the miR-23 similar to 27 similar to 24 similar to 2 superfamily. The role of miR-23a/b-3p in regulating hepatic lipid accumulation is still unknown. Here, we found that increased miR-23a-3p and miR-23b-3p levels were accompanied by an increase in the protein levels of the sterol regulatory element-binding protein-1 (SREBP-1) and fatty acid synthase (FAS) in the steatotic livers of mice fed a high-fat diet and leptin receptor-deficient type 2 diabetic mice (db/db). Importantly, overexpression of miR-23a/b-3p in Hep1-6 cells elevated the intracellular triglyceride level and upregulated the expression of Srebp-1c and Fas. Taken together, these results suggested that miR-23a/b-3p enhanced mRNA stability by binding the 5'-UTR of Srebp-1c and Fas mRNA, thereby promoting triglyceride accumulation in hepatocytes.