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肠易激综合征的异常肠-脑信号传递——胆汁酸的作用。

Aberrant Gut-To-Brain Signaling in Irritable Bowel Syndrome - The Role of Bile Acids.

机构信息

Department of Physiology, College of Medicine and Health, University College Cork, Cork, Ireland.

APC Microbiome Ireland, University College Cork, Cork, Ireland.

出版信息

Front Endocrinol (Lausanne). 2021 Nov 30;12:745190. doi: 10.3389/fendo.2021.745190. eCollection 2021.

DOI:10.3389/fendo.2021.745190
PMID:34917022
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8669818/
Abstract

Functional bowel disorders such as irritable bowel syndrome (IBS) are common, multifactorial and have a major impact on the quality of life of individuals diagnosed with the condition. Heterogeneity in symptom manifestation, which includes changes in bowel habit and visceral pain sensitivity, are an indication of the complexity of the underlying pathophysiology. It is accepted that dysfunctional gut-brain communication, which incorporates efferent and afferent branches of the peripheral nervous system, circulating endocrine hormones and local paracrine and neurocrine factors, such as host and microbially-derived signaling molecules, underpins symptom manifestation. This review will focus on the potential role of hepatic bile acids in modulating gut-to-brain signaling in IBS patients. Bile acids are amphipathic molecules synthesized in the liver, which facilitate digestion and absorption of dietary lipids. They are also important bioactive signaling molecules however, binding to bile acid receptors which are expressed on many different cell types. Bile acids have potent anti-microbial actions and thereby shape intestinal bacterial profiles. In turn, bacteria with bile salt hydrolase activity initiate the critical first step in transforming primary bile acids into secondary bile acids. Individuals with IBS are reported to have altered microbial profiles and modified bile acid pools. We have assessed the evidence to support a role for bile acids in the pathophysiology underlying the manifestation of IBS symptoms.

摘要

功能性肠病,如肠易激综合征(IBS),较为常见,具有多因素特征,且对患者的生活质量有重大影响。症状表现存在异质性,包括排便习惯改变和内脏疼痛敏感性,这表明其潜在病理生理学的复杂性。人们普遍认为,包括外周神经系统传出和传入分支、循环内分泌激素以及局部旁分泌和神经分泌因子(如宿主和微生物衍生的信号分子)在内的肠道-大脑功能障碍性通讯是症状表现的基础。本综述将重点关注肝胆汁酸在调节 IBS 患者肠道-大脑信号转导中的潜在作用。胆汁酸是在肝脏中合成的两亲性分子,有助于膳食脂质的消化和吸收。然而,它们也是重要的生物活性信号分子,与表达在许多不同细胞类型上的胆汁酸受体结合。胆汁酸具有强大的抗菌作用,从而塑造肠道细菌的特征。反过来,具有胆盐水解酶活性的细菌则启动了将初级胆汁酸转化为次级胆汁酸的关键第一步。有报道称,IBS 患者的微生物特征和胆汁酸池发生了改变。我们评估了支持胆汁酸在 IBS 症状表现的病理生理学中的作用的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/8669818/bd71fe10fdd3/fendo-12-745190-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/8669818/4249c7e8717a/fendo-12-745190-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/8669818/bd71fe10fdd3/fendo-12-745190-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/8669818/4249c7e8717a/fendo-12-745190-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f019/8669818/bd71fe10fdd3/fendo-12-745190-g002.jpg

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