Biochemistry Department, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, I.R Iran.
Arch Physiol Biochem. 2022 Apr;128(2):333-340. doi: 10.1080/13813455.2019.1680700. Epub 2019 Nov 5.
Here, we aimed to investigate whether the beneficial effects of metformin on lipid accumulation is mediated through regulation of miR-33b.
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.
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.
These findings suggest that metformin attenuates high glucose-induced lipid accumulation in HepG2 cell by downregulating the expression of miR-33b.
本研究旨在探讨二甲双胍是否通过调节 miR-33b 对脂质积累产生有益影响。
采用实时 PCR 和 Western blot 分别评估基因和 miRNA 的表达以及蛋白水平。为了研究 miR-33b 在脂质积累中的潜在作用，将 miR-33b 的模拟物转染到 HepG2 细胞中。
我们发现，二甲双胍通过抑制 SREBP1c 和 FAS，增加 CPT1 和 CROT 的表达，减少高糖诱导的 HepG2 细胞内脂质积累。miR-33b 的过表达显著阻止了二甲双胍对脂质含量和内、外甘油三酯水平的降低作用。重要的是，miR-33b 模拟物抑制了二甲双胍对 CPT1 和 CROT 表达的上调作用。
这些发现表明，二甲双胍通过下调 miR-33b 的表达来减轻高糖诱导的 HepG2 细胞内脂质积累。
