摘要
肥胖患者肝脏中过量的脂质堆积可引起肝细胞内质网应激、线粒体功能紊乱和脂毒性,该作用与胰岛素抵抗(IR)和非酒精性脂肪肝病(NALFLD)等代谢紊乱疾病的发生密切相关.自噬是细胞对内外持续性刺激的非损伤性应答反应,具有维持细胞结构和代谢平衡的功能.研究发现,自噬参与降解肝细胞内过多的脂质堆积,维持肝脏脂质代谢稳态.本文介绍了自噬调节肝脏脂质代谢的分子作用机制.
It has been well demonstrated that lipid accumulation in liver of the obesity is involved in endoplasmic reticulum stress,mitochondria dysfunction,and lipotoxicity,which is associated with insulin resistance( IR) and nonalcoholic fatty liver disease( NAFLD). Autophagy has been considered to be an adaptive response to stress,contributing to cellular homeostasis. It has been found that autophagy is activated during hepatic lipid accumulation. Autophagy plays an essential role in maintaining hepatic lipid metabolism. This review summarizes recent studies to identify the molecular mechanism of autophagy maintaining hepatic lipid metabolism in the obesity.
出处
《中国科学院大学学报(中英文)》
CSCD
北大核心
2016年第4期570-575,共6页
Journal of University of Chinese Academy of Sciences
基金
国家自然科学基金(11075207
20871120)
中国科学院科教融合项目(KJRH2015-003)
中国科学院知识创新工程重大项目(KSCX2-EW-J-29)资助
关键词
肥胖
肝脏
自噬
脂质代谢
obesity
liver
autophagy
lipid metabolism