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J Agric Food Chem. 2019 Jul 10;67(27):7726-7737. doi: 10.1021/acs.jafc.9b02523. Epub 2019 Jun 25.

Polyphenol-Rich Loquat Fruit Extract Prevents Fructose-Induced Nonalcoholic Fatty Liver Disease by Modulating Glycometabolism, Lipometabolism, Oxidative Stress, Inflammation, Intestinal Barrier, and Gut Microbiota in Mice.

Author information

1
School of Life Science and Biotechnology , Yangtze Normal University , Chongqing 408100 , China.
2
School of Aerospace Medicine , Fourth Military Medical University , Xi'an 710032 , China.
3
Department of Cardiology , First Affiliated Hospital of Xinjiang Medical University , Urumqi , China.
4
Xinjiang Key Laboratory of Cardiovascular Disease Research , Urumqi , China.
5
Chongqing Collaborative Innovation Center for Functional Food , Chongqing University of Education , Chongqing 400067 , China.

Abstract

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.

KEYWORDS:

fructose; gut microbiota; loquat fruit; nonalcoholic fatty liver disease; polyphenol

PMID:
31203627
DOI:
10.1021/acs.jafc.9b02523

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