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肝细胞特定的O-GlcNAc转移酶下调调节通过改善线粒体功能来改善非酒精性脂肪肝炎

Maria J Gonzalez-Rellan¹, Tamara Parracho², Violeta Heras²

¹Department of Physiology, CIMUS, University of Santiago de Compostela, Spain; CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERobn), Spain.

Molecular metabolism

|July 15, 2023

概括

不调节的O-GlcNAcylation是一种对营养素敏感的修饰,通过损害线粒体功能和增加肝脂肪来加剧非酒精性脂肪性肝病 (NAFLD). 抑制O-GlcNAc转移酶 (OGT) 显示了NAFLD的治疗潜力.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
代谢疾病代谢疾病

背景情况:

O-GlcNAcylation是一种动态的翻译后修饰,将营养代谢与细胞信号联系起来.
异常的O-GlcNAcylation与癌症,糖尿病和心血管疾病等疾病有关.
在非酒精性脂肪肝 (NAFLD) 病原体中O-GlcNAcylation的特定作用需要进一步阐明治疗向.

研究的目的:

调查O结合的N-乙糖胺 (O-GlcNAc) 转移酶 (OGT) 和O-GlcNAcylation在NAFLD的发展和进展中的作用.
探索OGT作为NAFLD的潜在治疗点.

主要方法:

利用初级小鼠肝细胞,人类肝细胞系,以及肝炎的体内小鼠模型.
在细胞和动物模型中操纵了OGT表达和活性.
从NAFLD患者和对照组的肝样本中分析了OGT和O-GlcNAcylation水平.
进行蛋白质组学以识别超O-GlcNAcylated蛋白质,特别是在线粒体中.

主要成果:

发现O-GlcNAcylation在患有脂肪肝炎的个体和动物模型的肝脏上调.
降低肝细胞中的OGT水平改善了食诱导的肝损伤在体外和体内.
在NAFLD肝脏中,线粒体蛋白质被确定为超-O-GlcNAcylated.
抑制OGT恢复了线粒体的氧化,并减少了肝脏脂质的积累.

结论:

放松O-GlcNAcylation的调节,特别是高O-GlcNAcylation,促进了NAFLD的进展.
这种促进是通过损害线粒体氧化和增强肝脏脂质积累来实现的.
针对OGT是一个有前途的治疗策略来管理NAFLD.

关键词:

线粒体功能障碍线粒体功能障碍这是NAFLD.这是一种O-GlcNAcylation.

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