期刊
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 67, 期 27, 页码 7726-7737出版社
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.9b02523
关键词
loquat fruit; polyphenol; fructose; nonalcoholic fatty liver disease; gut microbiota
资金
- Science and Technology Research Program of Chongqing Municipal Education Commission [KJQN201801436]
- Construction project of the Chongqing Collaborative Innovation Center for Functional Food at the Chongqing University of Education
Fructose as a daily sweetener is widely recognized as a risk catalyst for nonalcoholic fatty liver disease (NAFLD). The aim of current study is to evaluate the effects and molecular mechanism by which polyphenol-rich loquat fruit extract (LFP) prevents NAFLD in mice fed 30% fructose water (HF) for 8 weeks. Administration of LFP to HF-fed mice mitigated abnormal body weight, disordered lipid metabolism, oxidative stress, and inflammation through a mechanism regulated by the AKT, ChREBP/SREBP-1c, Nrf2, and TLR4/MyD88/TRIF pathways. LFP caused a significant decrease in the endotoxin content (16.67-12.7 EU/mL) in the liver of HF-fed mice. LFP not only improved HF-induced breakage of the intestinal barrier via interacting with tight junction proteins (ZO-1, occludin), mucin, and immunoreaction in the colon but also maintained normal colonic Firmicutes/Bacteroidetes ratios and the relative abundance of Veillonella in HF-fed mice. Our results suggest that LFP may serve as a nutritional agent for protecting liver in HF-fed mice.
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