Impaired Intestinal Akkermansia muciniphila and Aryl Hydrocarbon Receptor Ligands Contribute to Nonalcoholic Fatty Liver Disease in Mice.
Zunji Shi,Zunji Shi,Hehua Lei,Gui Chen,Peihong Yuan,Zheng Cao,Hooi-Leng Ser,Xuehang Zhu,Fang Wu,Caixiang Liu,Manyuan Dong,Yuchen Song,Yangyang Guo,Chuan Chen,Kexin Hu,Yifan Zhu,Xin An Zeng,Jinlin Zhou,Yu-Jing Lu,Andrew D. Patterson,Limin Zhang +20 more
- Vol. 6, Iss: 1
TLDR
In this article, the authors identify a mechanism linking intestinal Akkermansia muciniphila and the aryl hydrocarbon receptor (AHR) to saccharin/sucralose-induced nonalcoholic fatty liver disease (NAFLD) in mice.Abstract:
Noncaloric artificial sweeteners (NAS) are extensively introduced into commonly consumed drinks and foods worldwide. However, data on the health effects of NAS consumption remain elusive. Saccharin and sucralose have been shown to pass through the human gastrointestinal tract without undergoing absorption and metabolism and directly encounter the gut microbiota community. Here, we aimed to identify a novel mechanism linking intestinal Akkermansia muciniphila and the aryl hydrocarbon receptor (AHR) to saccharin/sucralose-induced nonalcoholic fatty liver disease (NAFLD) in mice. Saccharin/sucralose consumption altered the gut microbial community structure, with significant depletion of A. muciniphila abundance in the cecal contents of mice, resulting in disruption of intestinal permeability and a high level of serum lipopolysaccharide, which likely contributed to systemic inflammation and caused NAFLD in mice. Saccharin/sucralose also markedly decreased microbiota-derived AHR ligands and colonic AHR expression, which are closely associated with many metabolic syndromes. Metformin or fructo-oligosaccharide supplementation significantly restored A. muciniphila and AHR ligands in sucralose-consuming mice, consequently ameliorating NAFLD.IMPORTANCE Our findings indicate that the gut-liver signaling axis contributes to saccharin/sucralose consumption-induced NAFLD. Supplementation with metformin or fructo-oligosaccharide is a potential therapeutic strategy for NAFLD treatment. In addition, we also developed a new nutritional strategy by using a natural sweetener (neohesperidin dihydrochalcone [NHDC]) as a substitute for NAS and free sugars.read more
Citations
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The Function of Xenobiotic Receptors in Metabolic Diseases
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Akkermansia muciniphila Enhances Egg Quality and the Lipid Profile of Egg Yolk by Improving Lipid Metabolism
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Journal ArticleDOI
Alterations of the human gut microbiome in liver cirrhosis
Nan Qin,Fengling Yang,Ang Li,Edi Prifti,Yanfei Chen,Li Shao,Jing Guo,Jian Yao,Lingjiao Wu,Jiawei Zhou,Ni Shujun,Lin Liu,Nicolas Pons,Jean-Michel Batto,Sean Kennedy,Pierre Leonard,Chunhui Yuan,Wenchao Ding,Yuanting Chen,Xinjun Hu,Beiwen Zheng,Guirong Qian,Wei Xu,S. Dusko Ehrlich,Shu-Sen Zheng,Lanjuan Li +25 more
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Journal ArticleDOI
Tryptophan Catabolites from Microbiota Engage Aryl Hydrocarbon Receptor and Balance Mucosal Reactivity via Interleukin-22
Teresa Zelante,Rossana G. Iannitti,Cristina Cunha,Antonella De Luca,Gloria Giovannini,Giuseppe Pieraccini,Riccardo Zecchi,Carmen D'Angelo,Cristina Massi-Benedetti,Francesca Fallarino,Agostinho Carvalho,Paolo Puccetti,Luigina Romani +12 more
TL;DR: A metabolic pathway whereby Trp metabolites from the microbiota balance mucosal reactivity in mice is described, whereby highly adaptive lactobacilli are expanded and produce an aryl hydrocarbon receptor (AhR) ligand-indole-3-aldehyde-that contributes to AhR-dependent Il22 transcription.
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