Walnut green husk polysaccharides prevent obesity, chronic inflammatory responses, nonalcoholic fatty liver disease and colonic tissue damage in high-fat diet fed rats

被引:64
作者
Wang, Guoliang [1 ]
Yang, Xiaoyue [1 ]
Wang, Jing [1 ]
Zhong, Diying [1 ]
Zhang, Runguang [1 ]
Zhang, Yani [1 ]
Feng, Luoluo [1 ]
Zhang, Youlin [1 ]
机构
[1] Shaanxi Normal Univ, Coll Food Engn & Nutr Sci, Xian 710119, Peoples R China
关键词
Walnut green husk polysaccharide; Inflammation; Obesity; Gut microbiota; Short chain fatty acids; BROWN ADIPOSE-TISSUE; VASCULAR ENDOTHELIAL DYSFUNCTION; GUT MICROBIOTA; INTESTINAL PERMEABILITY; SIGNALING PATHWAYS; OXIDATIVE STRESS; ACIDS; ACTIVATION; HEALTH; ASSOCIATION;
D O I
10.1016/j.ijbiomac.2021.04.047
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
High-fat (HF) diets cause obesity, gut microbial dysbiosis and associated disorders and inflammatory bowel disease (IBD) due to increased intestinal permeability, which is an important reason for chronic inflammation and oxidative stress. This study was to investigate the effects and mechanism by which walnut green husk polysaccharides (WGHP) prevents obesity, oxidative stress, inflammation, liver and colon damage in HF diet induced rats. We found that WGHP alleviated HF-induced abnormal weight gain, disordered lipid metabolism, inflammation, oxidative stress, colonic tissue injury and up-regulate the expression level of colonic tight junction protein in the rats. Besides, the administration of WGHP promoted browning of iWAT and thermogenesis in BAT of HF-fed rats, and improved gut microbiota dysbiosis by increasing the bacterial diversity and reducing the relative abundance of potential pathogenic bacteria in the colon of the rats. Furthermore, WGHP consumption not only increased the SCFAs content but also improved the relative abundance of Prevotellaceae and Allobaculum in the gut of rats. Our results suggest that the protective effect of WGHP on metabolic inflammation caused by HF may be due to the regulation of gut microbiota and SCFAs. (c) 2021 Elsevier B.V. All rights reserved.
引用
收藏
页码:879 / 898
页数:20
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