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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.
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页数:10
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