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源自 - 的细胞外囊泡对HepG2细胞葡萄糖代谢及胰岛素抵抗诱导的影响。

The effect of -derived extracellular vesicles on glucose metabolism and induction of insulin resistance in HepG2 cells.

作者信息

Talebi Ghazaleh, Saffarian Parvaneh, Hakemi-Vala Mojdeh, Sadeghi Amir, Yadegar Abbas

机构信息

Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.

Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

出版信息

Arch Physiol Biochem. 2025 Apr;131(2):316-327. doi: 10.1080/13813455.2024.2418494. Epub 2024 Oct 21.

DOI:10.1080/13813455.2024.2418494
PMID:39431628
Abstract

infection has been associated with the development of insulin resistance (IR). This study aimed to examine the effect of -derived extracellular vesicles (EVs) on IR induction. EVs were derived from two strains, and characterised by transmission electron microscopy and dynamic light scattering. Different concentrations of insulin were added to HepG2 cells to induce IR model. HepG2 cells were exposed to various concentrations of -derived EVs to assess IR development. The gene expression of , , , , , and miR-140 was examined using RT-qPCR. Glucose uptake analysis revealed insulin at 5 × 10 mol/l and EVs at 50 µg/ml induced IR model in HepG2 cells. -derived EVs downregulated the expression level of , , and , and upregulated , , , and miR-140 expression in HepG2 cells. In conclusion, our findings propose a novel mechanism by which derived EVs could potentially induce IR.

摘要

感染与胰岛素抵抗(IR)的发生有关。本研究旨在探讨[具体细菌名称]来源的细胞外囊泡(EVs)对IR诱导的影响。EVs来源于两种[具体细菌名称]菌株,并通过透射电子显微镜和动态光散射进行表征。向HepG2细胞中添加不同浓度的胰岛素以诱导IR模型。将HepG2细胞暴露于不同浓度的[具体细菌名称]来源的EVs中,以评估IR的发展。使用RT-qPCR检测[相关基因名称]、[相关基因名称]、[相关基因名称]、[相关基因名称]、[相关基因名称]、[相关基因名称]和miR-140的基因表达。葡萄糖摄取分析显示,5×10⁻⁶mol/l的胰岛素和50μg/ml的EVs可诱导HepG2细胞中的IR模型。[具体细菌名称]来源的EVs下调了HepG2细胞中[相关基因名称]、[相关基因名称]和[相关基因名称]的表达水平,并上调了[相关基因名称]、[相关基因名称]、[相关基因名称]和miR-140的表达。总之,我们的研究结果提出了一种新的机制,即[具体细菌名称]来源的EVs可能潜在地诱导IR。

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