摘要
非酒精性脂肪肝(NAFLD)的病理与脂毒性密切相关。血中游离脂肪酸(freefatty acid,FFA)水平过高,瘦素代偿调节脂质氧化功能失调,造成FFA沉积在肝脏,导致肝细胞脂毒性,发生脂性凋亡。其凋亡机制主要与线粒体、溶酶体、Fas及内质网应激有关。降低血中FFA浓度,减少FFA在肝细胞的沉积,增加FFA的氧化能防止脂毒性的发生。开发改变脂肪酸代谢,降低脂毒性的药物将有很大的应用前景。
Objective:Lipotoxicity is crucial to the pathogenesis of nonalcoholic fatty liver disease(NAFLD).If liver is exposed to an excess of free fatty acids in blood,unless leptin action increases their oxidation sufficiently,unoxidized fatty acids will deposit in hepatocytes and cause lipotoxicity and lipoapoptosis.The mechanisms of this programmed cell death involve mitochondrion and lysosomes dysfunction,Fas expression and endoplasmic reticulum(ER)stress.The measures to prevent lipotoxicity include decreasing l...
出处
《华西医学》
CAS
2008年第6期1482-1484,共3页
West China Medical Journal
关键词
游离脂肪酸
脂毒性
非酒精性脂肪肝
free fatty acids
lipotoxicity
nonalcoholic fatty liver disease
