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肠道微生物群-胆汁酸相互作用与腹泻型肠易激综合征

Gut Microbiota-Bile Acid Crosstalk in Diarrhea-Irritable Bowel Syndrome.

机构信息

The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou 510000, China.

Department of Gastroenterology, The Second People's Hospital of China Three Gorges University, Yichang 443000, China.

出版信息

Biomed Res Int. 2020 Nov 12;2020:3828249. doi: 10.1155/2020/3828249. eCollection 2020.

DOI:10.1155/2020/3828249
PMID:33274207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7676935/
Abstract

The occurrence of diarrhea-predominant irritable bowel syndrome (IBS-D) is the result of multiple factors, and its pathogenesis has not yet been clarified. Emerging evidence indicates abnormal changes in gut microbiota and bile acid (BA) metabolism have a close relationship with IBS-D. Gut microbiota is involved in the secondary BA production via deconjugation, 7-dehydroxylation, oxidation, epimerization, desulfation, and esterification reactions respectively. Changes in the composition and quantity of gut microbiota have an important impact on the metabolism of BAs, which can lead to the occurrence of gastrointestinal diseases. BAs, synthesized in the hepatocytes, play an important role in maintaining the homeostasis of gut microbiota and the balance of glucose and lipid metabolism. In consideration of the complex biological functional connections among gut microbiota, BAs, and IBS-D, it is urgent to review the latest research progress in this field. In this review, we summarized the alterations of gut microbiota in IBS-D and discussed the mechanistic connections between gut microbiota and BA metabolism in IBS-D, which may be involved in activating two important bile acid receptors, G-protein coupled bile acid receptor 1 (TGR5) and farnesoid X receptor (FXR). We also highlight the strategies of prevention and treatment of IBS-D via regulating gut microbiota-bile acid axis, including probiotics, fecal microbiota transplantation (FMT), cholestyramine, and the cutting-edge technology about bacteria genetic engineering.

摘要

腹泻型肠易激综合征(IBS-D)的发生是多种因素共同作用的结果,其发病机制尚未阐明。新出现的证据表明,肠道微生物群和胆汁酸(BA)代谢的异常变化与 IBS-D 密切相关。肠道微生物群通过去结合、7-脱羟化、氧化、差向异构化、脱硫和酯化反应分别参与次级 BA 的产生。肠道微生物群的组成和数量的变化对 BAs 的代谢有重要影响,可导致胃肠道疾病的发生。BA 在肝细胞中合成,在维持肠道微生物群的内稳态和葡萄糖及脂质代谢平衡方面发挥着重要作用。鉴于肠道微生物群、BAs 和 IBS-D 之间复杂的生物学功能联系,迫切需要综述该领域的最新研究进展。在这篇综述中,我们总结了 IBS-D 中肠道微生物群的改变,并讨论了肠道微生物群与 IBS-D 中 BA 代谢之间的机制联系,这可能涉及激活两个重要的胆汁酸受体,G 蛋白偶联胆汁酸受体 1(TGR5)和法尼醇 X 受体(FXR)。我们还强调了通过调节肠道微生物群-胆汁酸轴预防和治疗 IBS-D 的策略,包括益生菌、粪便微生物移植(FMT)、考来烯胺和细菌基因工程的前沿技术。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def9/7676935/485671017b23/BMRI2020-3828249.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def9/7676935/92c69a3eefa5/BMRI2020-3828249.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def9/7676935/485671017b23/BMRI2020-3828249.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def9/7676935/92c69a3eefa5/BMRI2020-3828249.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def9/7676935/485671017b23/BMRI2020-3828249.002.jpg

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