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Upregulation of miR-181a impairs lipid metabolism by targeting PPARα expression in nonalcoholic fatty liver disease.

Abstract：

:Recent studies have reported elevated expression of miR-181a in patients with non-alcoholic fatty liver disease (NAFLD), suggesting that it may play an important role in liver lipid metabolism and insulin resistance. We aimed to investigate the effect of miR-181a in lipid metabolism and find new treatments for NAFLD. The expression level of miR-181a in NAFLD patient serum and a palmitic acid (PA)-induced NAFLD cell model was examined by Q-PCR. Oil red O staining and triglyceride assays were used to assess lipid accumulation in hepatocytes. Western blotting was used to detect the protein expression levels of peroxisome proliferator-activated receptor-α (PPARα) and the fatty acid β-oxidation-related genes. Direct interactions were validated by dual-luciferase reporter gene assays. MiR-181a expression was significantly upregulated in the serum of NAFLD patients and PA-induced hepatocytes. Inhibition of miR-181a expression resulted in the increased expression of PPARα and its downstream genes, and PA-induced lipid accumulation in hepatocytes was also inhibited. Upregulation of miR-181a resulted in the downregulation of its direct target PPARα and downstream gene expression of PPARα as well as aggravated lipid accumulation in hepatocytes. At the same time, the increased expression of PPARα can offset lipid accumulation in hepatocytes induced by miR-181a mimics. This study demonstrates that reducing the expression of miR-181a may improve lipid metabolism in NAFLD. The downregulation of miR-181a expression can be a therapeutic strategy for NAFLD by modulating its target PPARα.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Huang R,Duan X,Liu X,Cao H,Wang Y,Fan J,Wang B

doi

10.1016/j.bbrc.2018.12.061

subject

Has Abstract

pub_date

2019-01-22 00:00:00

pages

1252-1258

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(18)32704-9

journal_volume

508

pub_type

杂志文章

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