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Metformin Reduces Lipid Accumulation in Hepg2 Cells Via Downregulation of Mir-33B Publisher Pubmed



Zare M1 ; Panahi G2 ; Koushki M2 ; Mostafavipour Z1, 3 ; Meshkani R2
Authors
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Authors Affiliations
  1. 1. Biochemistry Department, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
  2. 2. Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Maternal-Fetal Medicine Research Center, Shiraz University of Medical Sciences, Shiraz, Iran

Source: Archives of Physiology and Biochemistry Published:2022


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. © 2019 Informa UK Limited, trading as Taylor & Francis Group.
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