Alginate oligosaccharides improve high-fat induced hepatic steatosis via PGC-1α-mediated lipophagy and fatty acid β-oxidation pathway

被引:2
|
作者
Li, Zhuoyu [1 ]
Zhao, Mengyao [1 ]
Ji, Xiaoguo [1 ]
Fan, Liqiang [1 ]
Zhao, Liming [1 ,2 ]
机构
[1] East China Univ Sci & Technol, R&D Ctr Separat & Extract Technol Fermentat Ind, Sch Biotechnol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
[2] Shanghai Collaborat Innovat Ctr Biomfg Technol SCI, Shanghai 200237, Peoples R China
基金
上海市自然科学基金;
关键词
Alginate oligosaccharides (AOS); Non-alcoholic fatty liver disease (NAFLD); Lipid -lowering effect; PGC-1; alpha; LIVER-DISEASE; AUTOPHAGY; PATHOGENESIS; PREVALENCE;
D O I
10.1016/j.jff.2023.105825
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
This study explored the lipid-lowering effect and intervention mechanism of alginate oligosaccharides (AOS) on non-alcoholic fatty liver disease (NAFLD). Results showed that both unsaturated (UAOS) and saturated (SAOS) AOS improved the hepatic steatosis of NAFLD mice fed a high-fat diet (HFD). AOS promoted lipid catabolism in vivo and in vitro by activating the lipophagy and free fatty acid (FFA) 8 -oxidation pathways. Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha) represented the up-stream target of the FFA 8 -oxidation pathway and upregulated both in in vivo and in vitro, suggesting it might be the AOS intervention target. By activating or inhibiting PGC-1 alpha, AOS modulated the PGC-1 alpha activity to reduce hepatic lipid accumulation. Therefore, the results indicated that AOS exhibited a lipid-lowering effect via the PGC-1 alpha-mediated lipophagy-FFA 8 -oxidation transduction signal axis. These findings provided insight into using food-derived ingredients to intervene and treat chronic diseases involving lipid metabolism disorders.
引用
收藏
页数:10
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