详细信息
Chitobiose exhibited a lipid-lowering effect in ob/ob-/- mice via butyric acid enrolled liver-gut crosstalk ( SCI-EXPANDED收录 EI收录)
文献类型:期刊文献
英文题名:Chitobiose exhibited a lipid-lowering effect in ob/ob-/- mice via butyric acid enrolled liver-gut crosstalk
作者:Zhuang, Xinye[1];Zhao, Mengyao[1,3];Ji, Xiaoguo[1];Yang, Sihan[1];Yin, Hao[2];Zhao, Liming[1,2,3]
机构:[1]East China Univ Sci & Technol, Sch Biotechnol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Shanghai Changzheng Hosp, Organ Transplant Ctr, Shanghai, Peoples R China;[3]Shanghai Collaborat Innovat Ctr Biomfg Technol SCI, Shanghai 200237, Peoples R China
年份:2023
卷号:10
期号:1
外文期刊名:BIORESOURCES AND BIOPROCESSING
收录:;EI(收录号:20234615043859);WOS:【SCI-EXPANDED(收录号:WOS:001102040100001)】;
基金:Not applicable.
语种:英文
外文关键词:Chitobiose; Butyric acid; Non-alcoholic fatty liver disease; Lipid beta-oxidation; Liver-gut axis signaling
摘要:Chitobiose (COS2) efficiently lowers lipids in vivo and facilitates butyric acid enrichment during human fecal fermentation. However, whether COS2 can interact with butyric acid to generate a hypolipidemic effect remains unclear. This study examined the hypolipidemic mechanism of COS2 involving butyric acid, which could alleviate non-alcoholic fatty liver disease (NAFLD). The results revealed that COS2 administration modulated the beta-oxidation pathway in the liver and restructured the short chain fatty acids in the fecal of ob/ob(-/-) mice. Moreover, the hypolipidemic effect of COS2 and its specific accumulated metabolite butyric acid was verified in sodium oleate-induced HepG2 cells. Butyric acid was more effective to reverse lipid accumulation and up-regulate beta-oxidation pathway at lower concentrations. Furthermore, structural analysis suggested that butyric acid formed hydrogen bonds with key residues in hydrophilic ligand binding domains (LBDs) of PPAR alpha and activated the transcriptional activity of the receptor. Therefore, the potential mechanism behind the lipid-lowering effect of COS2 in vivo involved restoring hepatic lipid disorders via butyric acid accumulation and liver-gut axis signaling.
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