MUP1 mediates urolithin A alleviation of chronic alcohol-related liver disease via gut-microbiota-liver axis
文献类型： 外文期刊
作者： Zhang, Hongbo 1 ; Li, Chaoyue 1 ; Han, Lin 1 ; Xiao, Yao 1 ; Bian, Ji 2 ; Liu, Chao 3 ; Gong, Lan 4 ; Liu, Zhigang 1 ; Wang, Min 1 ;
作者机构： 1.Northwest A&F Univ, Coll Food Sci & Engn, Yang Ling 712100, Shaanxi, Peoples R China
2.Univ Sydney, Sydney, Australia
3.Shandong Acad Agr Sci, Inst Agrofood Sci & Technol, Key Lab Novel Food Resources Proc, Minist Agr & Rural Affairs, Jinan, Peoples R China
4.Univ New South Wales, UNSW Microbiome Res Ctr, St George & Sutherland Clin Campus, Sydney 2052, Australia
关键词： Alcohol-related liver disease; urolithin A; endoplasmic reticulum stress; MUP1 protein; gut-microbiota-liver axis
期刊名称：GUT MICROBES （ 影响因子：12.2； 五年影响因子：12.3 ）
ISSN： 1949-0976
年卷期： 2024 年 16 卷 1 期
页码：
收录情况： SCI
摘要： Alcohol-related liver disease (ALD) is recognized as a global health crisis, contributing to approximately 20% of liver cancer-associated fatalities. Dysbiosis of the gut microbiome is associated with the development of ALD, with the gut microbial metabolite urolithin A (UA) exhibiting a potential for alleviating liver symptoms. However, the protective efficacy of UA against ALD and its underlying mechanism mediated by microbiota remain elusive. In this study, we provide evidence demonstrating that UA effectively ameliorates alcohol-induced metabolic disorders and hepatic endoplasmic reticulum (ER) stress through a specific gut-microbiota-liver axis mediated by major urinary protein 1 (MUP1). Moreover, UA exhibited the potential to restore alcohol-induced dysbiosis of the intestinal microbiota by enriching the abundance of Bacteroides sartorii (B. sartorii), Parabacteroides distasonis (P. distasonis), and Akkermansia muciniphila (A. muciniphila), along with their derived metabolite propionic acid. Partial attenuation of the hepatoprotective effects exerted by UA was observed upon depletion of gut microbiota using antibiotics. Subsequently, a fecal microbiota transplantation (FMT) experiment was conducted to evaluate the microbiota-dependent effects of UA in ALD. FMT derived from mice treated with UA exhibited comparable efficacy to direct UA treatment, as it effectively attenuated ER stress through modulation of MUP1. It was noteworthy that strong associations were observed among the hepatic MUP1, gut microbiome, and metabolome profiles affected by UA. Intriguingly, oral administration of UA-enriched B. sartorii, P. distasonis, and A. muciniphila can enhance propionic acid production to effectively suppress ER stress via MUP1, mimicking UA treatment. Collectively, these findings elucidate the causal mechanism that UA alleviated ALD through the gut-microbiota-liver axis. This unique mechanism sheds light on developing novel microbiome-targeted therapeutic strategies against ALD. [GRAPHICS]
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