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HepG2细胞胰岛素抵抗模型的建立与评价

Establishment and Evaluation of HepG2 Cell Insulin Resistance Model.

作者信息

Meng Zixuan, Han Yuehua, Ruan Linda, Xu Chenming, Zhang Mengxiao, Liu Hao

机构信息

School of Pharmacy, Bengbu Medical University, Bengbu, People's Republic of China.

Anhui Province Engineering Technology Research Center of Biochemical Pharmaceutical, Bengbu, Anhui Province, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2025 Jul 29;18:2573-2584. doi: 10.2147/DMSO.S523821. eCollection 2025.

DOI:10.2147/DMSO.S523821
PMID:40755745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12317709/
Abstract

OBJECTIVE

Establishing HepG2 cell insulin resistance models using glucosamine, high glucose with high insulin and palmitic acid and briefly evaluating them to provide reliable models for insulin resistance research.

METHODS

Three methods were used to induce insulin resistance in HepG2 cells, and glucose uptake and consumption, glucose metabolism-related mRNA and p-AKT/AKT protein levels and RNA-seq were detected to compare the three induction methods.

RESULTS

Glucose consumption capacity was reduced after glucosamine and palmitic acid induction and did not change significantly after high glucose with high insulin induction. Glucose uptake capacity was not significantly changed after glucosamine and high glucose with high insulin induction and was reduced after palmitic acid induction. After high insulin stimulation, p-AKT/AKT levels were elevated in glucosamine and high glucose with high insulin induction and did not change significantly in palmitic acid induction. , , and were elevated after glucosamine and palmitic acid stimulation, and only PCK1 was elevated after high glucose with high insulin stimulation. The transcriptomes of cells induced by the three methods differed widely.

CONCLUSION

Treatment with 0.2 mM palmitic acid for 24 h is a simple and stable method to induce insulin resistance in HepG2 cells.

摘要

目的

利用氨基葡萄糖、高糖高胰岛素以及棕榈酸建立HepG2细胞胰岛素抵抗模型,并对其进行简要评估,为胰岛素抵抗研究提供可靠模型。

方法

采用三种方法诱导HepG2细胞产生胰岛素抵抗,检测葡萄糖摄取与消耗、葡萄糖代谢相关mRNA以及p-AKT/AKT蛋白水平,并进行RNA测序,以比较三种诱导方法。

结果

氨基葡萄糖和棕榈酸诱导后葡萄糖消耗能力降低,高糖高胰岛素诱导后葡萄糖消耗能力无显著变化。氨基葡萄糖和高糖高胰岛素诱导后葡萄糖摄取能力无显著变化,棕榈酸诱导后葡萄糖摄取能力降低。高胰岛素刺激后,氨基葡萄糖和高糖高胰岛素诱导组p-AKT/AKT水平升高,棕榈酸诱导组无显著变化。氨基葡萄糖和棕榈酸刺激后, 、 和 升高,高糖高胰岛素刺激后仅磷酸烯醇式丙酮酸羧激酶1(PCK1)升高。三种方法诱导的细胞转录组差异很大。

结论

用0.2 mM棕榈酸处理24小时是诱导HepG2细胞胰岛素抵抗的一种简单且稳定的方法。

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本文引用的文献

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Exogenous Nucleotides Ameliorate Insulin Resistance Induced by Palmitic Acid in HepG2 Cells through the IRS-1/AKT/FOXO1 Pathways.外源性核苷酸通过 IRS-1/AKT/FOXO1 通路改善棕榈酸诱导的 HepG2 细胞胰岛素抵抗。
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Berberine protects mice against type 2 diabetes by promoting PPARγ-FGF21-GLUT2-regulated insulin sensitivity and glucose/lipid homeostasis.小檗碱通过促进 PPARγ-FGF21-GLUT2 调控的胰岛素敏感性和糖脂稳态来保护小鼠免受 2 型糖尿病的影响。
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Tuning of cellular insulin release by music for real-time diabetes control.
通过音乐调节细胞胰岛素释放以实现糖尿病的实时控制。
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Ube4A maintains metabolic homeostasis and facilitates insulin signaling in vivo.UBE4A 维持代谢平衡并促进体内胰岛素信号传导。
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Insulin Resistance Model: A Recent Update.胰岛素抵抗模型:最新进展。
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