幽门螺杆菌衍生的细胞外囊泡对 HepG2 细胞葡萄糖代谢和诱导胰岛素抵抗的影响

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM Archives of Physiology and Biochemistry Pub Date : 2024-10-21 DOI:10.1080/13813455.2024.2418494

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

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引用次数: 0

摘要

幽门螺杆菌感染与胰岛素抵抗（IR）的发生有关。本研究旨在探讨幽门螺杆菌衍生的细胞外囊泡（EVs）对胰岛素抵抗诱导的影响。EVs来源于两种幽门螺杆菌菌株，并通过透射电子显微镜和动态光散射进行了表征。在HepG2细胞中加入不同浓度的胰岛素诱导IR模型。HepG2细胞暴露于不同浓度的幽门螺杆菌衍生的EVs，以评估IR的发展。使用 RT-qPCR 检测了 IRS1、AKT2、GLUT2、IL-6、SOCS3、c-Jun 和 miR-140 的基因表达。葡萄糖摄取分析表明，5 × 10 -7 mol/l的胰岛素和50 µg/ml的EVs可诱导HepG2细胞形成IR模型。幽门螺杆菌衍生的 EVs 下调了 HepG2 细胞中 IRS1、AKT2 和 GLUT2 的表达水平，并上调了 IL-6、SOCS3、c-Jun 和 miR-140 的表达。总之，我们的研究结果提出了幽门螺杆菌衍生的EV可能诱导IR的新机制。

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

Helicobacter pylori infection has been associated with the development of insulin resistance (IR). This study aimed to examine the effect of H. pylori-derived extracellular vesicles (EVs) on IR induction. EVs were derived from two H. pylori 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 H. pylori-derived EVs to assess IR development. The gene expression of IRS1, AKT2, GLUT2, IL-6, SOCS3, c-Jun and miR-140 was examined using RT-qPCR. Glucose uptake analysis revealed insulin at 5 × 10 ^-7mol/l and EVs at 50 µg/ml induced IR model in HepG2 cells. H. pylori-derived EVs downregulated the expression level of IRS1, AKT2, and GLUT2, and upregulated IL-6, SOCS3, c-Jun, and miR-140 expression in HepG2 cells. In conclusion, our findings propose a novel mechanism by which H. pylori-derived EVs could potentially induce IR.

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.