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微生物代谢产物三甲胺 N-氧化物与血管功能障碍和自身免疫性疾病类风湿关节炎有关。

The Microbial Metabolite Trimethylamine N-Oxide Links Vascular Dysfunctions and the Autoimmune Disease Rheumatoid Arthritis.

机构信息

Department of Microbiology and Immunology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.

Center for Inflammation, Translational and Clinical Lung Research, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.

出版信息

Nutrients. 2019 Aug 7;11(8):1821. doi: 10.3390/nu11081821.

Abstract

Diet and microbiota each have a direct impact on many chronic, inflammatory, and metabolic diseases. As the field develops, a new perspective is emerging. The effects of diet may depend on the microbiota composition of the intestine. A diet that is rich in choline, red meat, dairy, or egg may promote the growth, or change the composition, of microbial species. The microbiota, in turn, may produce metabolites that increase the risk of cardiovascular disease. This article reviews our current understanding of the effects of the molecule trimethylamine--oxide (TMAO) obtained from food or produced by the microbiota. We review the mechanisms of actions of TMAO, and studies that associate it with cardiovascular and chronic kidney diseases. We introduce a novel concept: TMAO is one among a group of selective uremic toxins that may rise to high levels in the circulation or accumulate in various organs. Based on this information, we evaluate how TMAO may harm, by exacerbating inflammation, or may protect, by attenuating amyloid formation, in autoimmune diseases such as rheumatoid arthritis.

摘要

饮食和微生物群都直接影响许多慢性、炎症性和代谢性疾病。随着该领域的发展,一种新的观点正在出现。饮食的影响可能取决于肠道的微生物群组成。富含胆碱、红肉、乳制品或蛋类的饮食可能会促进微生物种类的生长或改变其组成。微生物群反过来又可能产生增加心血管疾病风险的代谢物。本文综述了我们目前对食物中获得或由微生物群产生的分子三甲胺氧化物(TMAO)的影响的理解。我们综述了 TMAO 的作用机制,以及与心血管疾病和慢性肾病相关的研究。我们介绍了一个新的概念:TMAO 是一组选择性尿毒症毒素中的一种,它可能在循环中升高到高水平或在各种器官中积累。基于这些信息,我们评估了 TMAO 如何通过加重炎症来损害,以及如何通过减轻淀粉样蛋白形成来保护,在类风湿关节炎等自身免疫性疾病中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9bf8/6723051/246d97d9321b/nutrients-11-01821-g001.jpg

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