非酒精性脂肪肝
碳水化合物反应元件结合蛋白
封堵器
氧化应激
果糖
炎症
肠道菌群
脂肪肝
化学
内分泌学
内科学
生物化学
生物
紧密连接
医学
基因
转录因子
疾病
作者
Wenfeng Li,Hengli Yang,Qiang Zhao,Xv Wang,Jing Zhang,Xin Zhao
标识
DOI:10.1021/acs.jafc.9b02523
摘要
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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