| First Author | Zhang Z | Year | 2018 |
| Journal | Metabolism | Volume | 88 |
| Pages | 31-39 | PubMed ID | 30309516 |
| Mgi Jnum | J:295602 | Mgi Id | MGI:6454103 |
| Doi | 10.1016/j.metabol.2018.08.007 | Citation | Zhang Z, et al. (2018) Obesity-induced upregulation of miR-361-5p promotes hepatosteatosis through targeting Sirt1. Metabolism 88:31-39 |
| abstractText | OBJECTIVE: Obesity is associated with an increased risk of many metabolic disorders, including non-alcoholic fatty liver disease (NAFLD). However, the underlying mechanisms remain poorly understood. Recent studies have demonstrated that MicroRNA-mediated gene silencing plays an important role in hepatic triglyceride (TG) metabolism. In the present study, we aimed to investigate the pathological function of miR-361-5p in the development of NAFLD. METHODS: Expression levels of miR-361-5p was determined by quantitative real-time PCR in livers of obese mice and NAFLD patients. Liver tissues from mice with miR-361-5p overexpression or inhibition were collected and analyzed by TG contents, gene expression profile. RESULTS: Expression of miR-361-5p was increased in the livers of two obese mouse models and NAFLD subjects. Overexpression of miR-361-5p in C57BL/6 mice led to hepatosteatosis, whereas inhibition of miR-361-5p expression in db/db mice improved TG accumulation and insulin sensitivity. Mechanistically, we identified Sirt1 as a direct target gene of miR-361-5p and re-introduction of Sirt1 largely abolished the metabolic action of miR-361-5p. CONCLUSIONS: Our results demonstrated the role of miR-361-5p in the regulation of hepatic TG homeostasis, which may provide potential therapeutic target for hepatosteatosis. |
