Metformin reduces lipid accumulation in HepG2 cells via downregulation of miR-33b

Abstract

Introduction

Here, we aimed to investigate whether the beneficial effects of metformin on lipid accumulation is mediated through regulation of miR-33b.

Methods

The expression of the genes and miRNAs and protein levels were evaluated using real-time PCR and western blot, respectively. To investigate the potential role of miR-33b in lipid accumulation, the mimic of the miR-33b was transfected into HepG2 cells.

Results

We found that metformin reduces high glucose-induced lipid accumulation in HepG2 cells through inhibiting of SREBP1c and FAS and increasing the expression of CPT1 and CROT. Overexpression of miR-33b significantly prevented the decreasing effect of metformin on lipid content and intra and extra triglyceride levels. Importantly, miR-33b mimic inhibited the increasing effects of metformin on the expression of CPT1 and CROT.

Conclusion

These findings suggest that metformin attenuates high glucose-induced lipid accumulation in HepG2 cell by downregulating the expression of miR-33b.

Keywords:

• miRNA
• miR-33b lipogenesis
• metformin
• HepG2
• high glucose

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This study was done as a part of PhD thesis of Mina Zare and supported by grant No. 94–01-01–10462 from the office of Vice Chancellor for Research and the Committee for Advanced Biomedical Sciences, Shiraz University of Medical Sciences.