Berberine Directly Affects the Gut Microbiota to Promote Intestinal Farnesoid X Receptor Activation
文献类型:期刊论文
作者 | Patterson, Andrew D.2; Anitha, Mallappa2; Zhang, Jingtao2; Koo, Imhoi2; Nichols, Robert G.2; Gui, Wei2; Cai, Jingwei2; Tian, Yuan1,2 |
刊名 | DRUG METABOLISM AND DISPOSITION
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出版日期 | 2019-02-01 |
卷号 | 47期号:2页码:86-93 |
ISSN号 | 0090-9556 |
DOI | 10.1124/dmd.118.083691 |
英文摘要 | Intestinal bacteria play an important role in bile acid metabolism and in the regulation of multiple host metabolic pathways (e.g., lipid and glucose homeostasis) through modulation of intestinal farnesoid X receptor (FXR) activity. Here, we examined the effect of berberine (BBR), a natural plant alkaloid, on intestinal bacteria using in vitro and in vivo models. In vivo, the metabolomic response and changes in mouse intestinal bacterial communities treated with BBR (100 mg/kg) for 5 days were assessed using NMR- and mass spectrometry-based metabolomics coupled with multivariate data analysis. Short-term BBR exposure altered intestinal bacteria by reducing Clostridium cluster XIVa and IV and their bile salt hydrolase (BSH) activity, which resulted in the accumulation of taurocholic acid (TCA). The accumulation of TCA was associated with activation of intestinal FXR, which can mediate bile acid, lipid, and glucose metabolism. In vitro, isolated mouse cecal bacteria were incubated with three doses of BBR (0.1, 1, and 10 mg/ml) for 4 hours in an anaerobic chamber. NMR-based metabolomics combined with flow cytometry was used to evaluate the direct physiologic and metabolic effect of BBR on the bacteria. In vitro, BBR exposure not only altered bacterial physiology but also changed bacterial community composition and function, especially reducing BSH-expressing bacteria like Clostridium spp. These data suggest that BBR directly affects bacteria to alter bile acid metabolism and activate FXR signaling. These data provide new insights into the link between intestinal bacteria, nuclear receptor signaling, and xenobiotics. |
WOS关键词 | BILE-ACID METABOLISM ; NUCLEAR RECEPTOR ; SALT HYDROLASE ; EXPRESSION ; HOST ; MECHANISM ; MICE ; DIET |
资助项目 | Pennsylvania Department of Health [Tobacco Commonwealth Universal Research Enhancement Funds] ; National Institutes of Health National Library of Medicine[T32LM12415-1] ; U.S. Department of Agriculture National Institute of Food and Agriculture[2914-38420-21822] |
WOS研究方向 | Pharmacology & Pharmacy |
语种 | 英语 |
WOS记录号 | WOS:000457846400004 |
出版者 | AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS |
资助机构 | Pennsylvania Department of Health [Tobacco Commonwealth Universal Research Enhancement Funds] ; Pennsylvania Department of Health [Tobacco Commonwealth Universal Research Enhancement Funds] ; National Institutes of Health National Library of Medicine ; National Institutes of Health National Library of Medicine ; U.S. Department of Agriculture National Institute of Food and Agriculture ; U.S. Department of Agriculture National Institute of Food and Agriculture ; Pennsylvania Department of Health [Tobacco Commonwealth Universal Research Enhancement Funds] ; Pennsylvania Department of Health [Tobacco Commonwealth Universal Research Enhancement Funds] ; National Institutes of Health National Library of Medicine ; National Institutes of Health National Library of Medicine ; U.S. Department of Agriculture National Institute of Food and Agriculture ; U.S. Department of Agriculture National Institute of Food and Agriculture ; Pennsylvania Department of Health [Tobacco Commonwealth Universal Research Enhancement Funds] ; Pennsylvania Department of Health [Tobacco Commonwealth Universal Research Enhancement Funds] ; National Institutes of Health National Library of Medicine ; National Institutes of Health National Library of Medicine ; U.S. Department of Agriculture National Institute of Food and Agriculture ; U.S. Department of Agriculture National Institute of Food and Agriculture ; Pennsylvania Department of Health [Tobacco Commonwealth Universal Research Enhancement Funds] ; Pennsylvania Department of Health [Tobacco Commonwealth Universal Research Enhancement Funds] ; National Institutes of Health National Library of Medicine ; National Institutes of Health National Library of Medicine ; U.S. Department of Agriculture National Institute of Food and Agriculture ; U.S. Department of Agriculture National Institute of Food and Agriculture |
源URL | [http://ir.wipm.ac.cn/handle/112942/14319] ![]() |
专题 | 中国科学院武汉物理与数学研究所 |
通讯作者 | Patterson, Andrew D. |
作者单位 | 1.Univ Chinese Acad Sci, Natl Ctr Magnet Resonance Wuhan, Key Lab Magnet Resonance Biol Syst,Chinese Acad S, Wuhan Inst Phys & Math,State Key Lab Magnet Res &, Wuhan, Hubei, Peoples R China 2.Penn State Univ, Dept Vet & Biomed Sci, 322 Life Sci Bldg, University Pk, PA 16802 USA |
推荐引用方式 GB/T 7714 | Patterson, Andrew D.,Anitha, Mallappa,Zhang, Jingtao,et al. Berberine Directly Affects the Gut Microbiota to Promote Intestinal Farnesoid X Receptor Activation[J]. DRUG METABOLISM AND DISPOSITION,2019,47(2):86-93. |
APA | Patterson, Andrew D..,Anitha, Mallappa.,Zhang, Jingtao.,Koo, Imhoi.,Nichols, Robert G..,...&Tian, Yuan.(2019).Berberine Directly Affects the Gut Microbiota to Promote Intestinal Farnesoid X Receptor Activation.DRUG METABOLISM AND DISPOSITION,47(2),86-93. |
MLA | Patterson, Andrew D.,et al."Berberine Directly Affects the Gut Microbiota to Promote Intestinal Farnesoid X Receptor Activation".DRUG METABOLISM AND DISPOSITION 47.2(2019):86-93. |
入库方式: OAI收割
来源:武汉物理与数学研究所
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