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肝脏IL22RA1缺乏症通过调节肝脏中的氧化来促进肝脏肥胖症

Yeping Huang¹, Fan Yu¹, Yue Ding²

¹Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Centre for Diabetes, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Hepatology (Baltimore, Md.)

|July 10, 2024

概括

介素-22受体α1 (IL22RA1) 对于维持肝脏健康至关重要. 它在肝细胞中的缺乏通过增加氧醇,促进脂质积累和NAFLD进展,突出了一个新的治疗点.

科学领域:

肝病学肝病学是一种肝病学.
代谢疾病代谢疾病
免疫学免疫学免疫学

背景情况:

非酒精性脂肪性肝病 (NAFLD) 是由脂质代谢失衡驱动的.
脂质平衡的肝脏内调节剂尚未完全理解.
干白素-22 (IL-22) 在NAFLD中表现出保护作用,但其在肝脂代谢中的具体作用尚不清楚.

研究的目的:

研究IL-22受体α1 (IL22RA1) 在调节肝脂代谢中的作用.
阐明 IL22RA1 缺乏影响肝脂平衡的分子机制.

主要方法:

在肝细胞和NAFLD模型中研究IL22RA1表达.
使用肝细胞特异性的Il22ra1淘汰赛小鼠.
分析了脂质积累,脂质生成,氧胆固醇水平以及相关的信号通路 (ATF3/CYP7B1,LXRα).

主要成果:

肝脏IL22RA1在NAFLD条件下下调.
肝细胞特异的Il22ra1淘汰赛小鼠发生了肝硬化症,胰岛素抵抗和炎症.
缺乏导致3β-基-5-胆固醇酸 (3β HCA) 通过ATF3/CYP7B1轴积累的脂质生成增加.
治疗IL-22减弱了3β HCA诱导的脂质发生.

结论:

肝脏IL22RA1对于维持脂质平衡至关重要.
IL22RA1通过ATF3/CYP7B1途径和3β HCA积累来调节肝脂代谢.
这项研究将3β HCA与肝脂平衡联系起来,并确定IL22RA1是关键调节剂.

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