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在HepG2细胞中诱导胰岛素抵抗的棕酸毒性的表征

Sajad Malik¹, Shrirang Inamdar¹, Jhankar Acharya¹

¹Department of Zoology, Savitribai Phule Pune University, Ganeshkhind, Pune 411007, India.

Toxicology in vitro : an international journal published in association with BIBRA

|March 2, 2024

概括

棕酸通过同时ROS-JNK和脂质-PKCε激活通路诱导胰岛素抵抗 (IR). 必须跨越HepG2细胞的值才能触发这种病态状态.

科学领域:

细胞生物学细胞生物学
代谢障碍代谢障碍代谢障碍
生物化学生化学

背景情况:

棕酸 (PA) 与胰岛素抵抗 (IR) 有关.
提出了两个机制:ROS诱导的JNK激活和脂质诱导的PKCε激活.
这些机制在PA诱导的IR中的相互作用尚不清楚.

研究的目的:

在肝细胞中描述PA诱导的IR.
调查JNK和PKCε在PA引起的IR中的作用.
阐明PA诱导的IR中涉及的信号通路.

主要方法:

经过8小时或16小时的治疗,HepG2细胞接受了不同度的PA治疗.
通过测量葡萄糖输出来评估胰岛素反应.
分析了关键信号蛋白 (JNK,PKCε,AKT,GSK3β,FOXO1) 和酶表达.

主要成果:

16小时的PA治疗,但不是8小时,在更高度的HepG2细胞中诱导了IR.
PA增加了ROS和脂质积累,分别激活了JNK和PKCε.
激活的JNK和PKCε导致IRS1酸化,AKT抑制,以及随后的GSK3β无活化,减少了糖原合成.

结论:

在PA诱导的IR中,ROS-JNK和脂质-PKCε通路同时运行.
为了在HepG2细胞中诱导IR,需要特定的PA暴露值.
由PA诱导的IR涉及AKT的抑制和随后通过FOXO1激活的肝脏葡萄糖生成的失调.

关键词:

胰岛素耐药性胰岛素耐药性是一种脂质的积累脂质的积累棕酸是一种棕酸.有反应性氧物种的反应性氧物种.

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