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肠道微生物群作为肥胖和 2 型糖尿病代谢性炎症的触发因素。

Gut Microbiota as a Trigger for Metabolic Inflammation in Obesity and Type 2 Diabetes.

机构信息

Department of Internal Medicine, Amsterdam University Medical Center (UMC), Vrije Universiteit (VU) University Medical Center, Amsterdam, Netherlands.

Department of Experimental Vascular Medicine, Amsterdam University Medical Center (UMC), Academic Medical Center, Amsterdam, Netherlands.

出版信息

Front Immunol. 2020 Oct 16;11:571731. doi: 10.3389/fimmu.2020.571731. eCollection 2020.

DOI:10.3389/fimmu.2020.571731
PMID:33178196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7596417/
Abstract

The gut microbiota has been linked to the development of obesity and type 2 diabetes (T2D). The underlying mechanisms as to how intestinal microbiota may contribute to T2D are only partly understood. It becomes progressively clear that T2D is characterized by a chronic state of low-grade inflammation, which has been linked to the development of insulin resistance. Here, we review the current evidence that intestinal microbiota, and the metabolites they produce, could drive the development of insulin resistance in obesity and T2D, possibly by initiating an inflammatory response. First, we will summarize major findings about immunological and gut microbial changes in these metabolic diseases. Next, we will give a detailed view on how gut microbial changes have been implicated in low-grade inflammation. Lastly, we will critically discuss clinical studies that focus on the interaction between gut microbiota and the immune system in metabolic disease. Overall, there is strong evidence that the tripartite interaction between gut microbiota, host immune system and metabolism is a critical partaker in the pathophysiology of obesity and T2D.

摘要

肠道微生物群与肥胖和 2 型糖尿病(T2D)的发展有关。肠道微生物群如何促进 T2D 的潜在机制尚不完全清楚。越来越明显的是,T2D 的特征是慢性低度炎症状态,这与胰岛素抵抗的发展有关。在这里,我们回顾了目前的证据,即肠道微生物群及其产生的代谢物可能通过引发炎症反应,导致肥胖和 T2D 中的胰岛素抵抗。首先,我们将总结这些代谢疾病中免疫和肠道微生物变化的主要发现。接下来,我们将详细讨论肠道微生物变化如何与低度炎症有关。最后,我们将批判性地讨论关注肠道微生物群与代谢疾病中免疫系统相互作用的临床研究。总的来说,有强有力的证据表明,肠道微生物群、宿主免疫系统和代谢之间的三方相互作用是肥胖和 T2D 病理生理学的一个关键参与者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f05b/7596417/cbffaa1253ca/fimmu-11-571731-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f05b/7596417/a07fd4656f6c/fimmu-11-571731-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f05b/7596417/3b9a9e073e5e/fimmu-11-571731-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f05b/7596417/c28c3f0ba1c2/fimmu-11-571731-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f05b/7596417/cbffaa1253ca/fimmu-11-571731-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f05b/7596417/a07fd4656f6c/fimmu-11-571731-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f05b/7596417/3b9a9e073e5e/fimmu-11-571731-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f05b/7596417/c28c3f0ba1c2/fimmu-11-571731-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f05b/7596417/cbffaa1253ca/fimmu-11-571731-g0005.jpg

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