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肠道微生物群、肥胖与糖尿病

Gut microbiota, obesity and diabetes.

作者信息

Patterson Elaine, Ryan Paul M, Cryan John F, Dinan Timothy G, Ross R Paul, Fitzgerald Gerald F, Stanton Catherine

机构信息

APC Microbiome Institute, University College Cork, Co. Cork, Ireland Food Biosciences Department, Teagasc Food Research Centre, Fermoy, Co. Cork, Ireland.

Food Biosciences Department, Teagasc Food Research Centre, Fermoy, Co. Cork, Ireland School of Microbiology, University College Cork, Co. Cork, Ireland.

出版信息

Postgrad Med J. 2016 May;92(1087):286-300. doi: 10.1136/postgradmedj-2015-133285. Epub 2016 Feb 24.

Abstract

The central role of the intestinal microbiota in the progression and, equally, prevention of metabolic dysfunction is becoming abundantly apparent. The symbiotic relationship between intestinal microbiota and host ensures appropriate development of the metabolic system in humans. However, disturbances in composition and, in turn, functionality of the intestinal microbiota can disrupt gut barrier function, a trip switch for metabolic endotoxemia. This low-grade chronic inflammation, brought about by the influx of inflammatory bacterial fragments into circulation through a malfunctioning gut barrier, has considerable knock-on effects for host adiposity and insulin resistance. Conversely, recent evidence suggests that there are certain bacterial species that may interact with host metabolism through metabolite-mediated stimulation of enteric hormones and other systems outside of the gastrointestinal tract, such as the endocannabinoid system. When the abundance of these keystone species begins to decline, we see a collapse of the symbiosis, reflected in a deterioration of host metabolic health. This review will investigate the intricate axis between the microbiota and host metabolism, while also addressing the promising and novel field of probiotics as metabolic therapies.

摘要

肠道微生物群在代谢功能障碍的进展以及预防方面所起的核心作用正变得愈发明显。肠道微生物群与宿主之间的共生关系确保了人类代谢系统的正常发育。然而,肠道微生物群的组成及其功能的紊乱会破坏肠道屏障功能,而肠道屏障功能是代谢性内毒素血症的一个触发开关。这种由炎症性细菌碎片通过功能失调的肠道屏障进入血液循环所引发的低度慢性炎症,对宿主肥胖和胰岛素抵抗具有相当大的连锁反应。相反,最近的证据表明,某些细菌物种可能通过代谢物介导的对肠道激素和胃肠道以外的其他系统(如内源性大麻素系统)的刺激来与宿主代谢相互作用。当这些关键物种的丰度开始下降时,我们会看到共生关系的瓦解,这反映在宿主代谢健康的恶化上。本综述将研究微生物群与宿主代谢之间的复杂轴,同时也探讨益生菌作为代谢疗法这一有前景的新领域。

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