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2 型糖尿病中肠道微生物组的改变:仅仅是巧合吗?

Altered Gut Microbiota in Type 2 Diabetes: Just a Coincidence?

机构信息

Azienda Ospedaliero Universitaria, Sassari, Italy.

HUMANITAS Gradenigo, University of Turin, C.so Regina Margherita 8, 10132, Turin, Italy.

出版信息

Curr Diab Rep. 2018 Sep 13;18(10):98. doi: 10.1007/s11892-018-1057-6.

DOI:10.1007/s11892-018-1057-6
PMID:30215149
Abstract

PURPOSE OF REVIEW

In the last decade many studies have suggested an association between the altered gut microbiota and multiple systemic diseases including diabetes. In this review, we will discuss potential pathophysiological mechanisms, the latest findings regarding the mechanisms linking gut dysbiosis and type 2 diabetes (T2D), and the results obtained with experimental modulation of microbiota.

RECENT FINDINGS

In T2D, gut dysbiosis contributes to onset and maintenance of insulin resistance. Different strategies that reduce dysbiosis can improve glycemic control. Evidence in animals and humans reveals differences between the gut microbial composition in healthy individuals and those with T2D. Changes in the intestinal ecosystem could cause inflammation, alter intestinal permeability, and modulate metabolism of bile acids, short-chain fatty acids and metabolites that act synergistically on metabolic regulation systems contributing to insulin resistance. Interventions that restore equilibrium in the gut appear to have beneficial effects and improve glycemic control. Future research should examine in detail and in larger studies other possible pathophysiological mechanisms to identify specific pathways modulated by microbiota modulation and identify new potential therapeutic targets.

摘要

目的综述

在过去的十年中,许多研究表明肠道微生物群的改变与多种系统性疾病有关,包括糖尿病。在这篇综述中,我们将讨论潜在的病理生理机制、关于肠道菌群失调与 2 型糖尿病(T2D)之间关联的最新发现,以及通过实验调节微生物组获得的结果。

最近的发现

在 T2D 中,肠道菌群失调有助于胰岛素抵抗的发生和维持。减少菌群失调的不同策略可以改善血糖控制。动物和人类的证据揭示了健康个体和 T2D 患者肠道微生物组成的差异。肠道生态系统的变化可能导致炎症、改变肠道通透性,并调节胆汁酸、短链脂肪酸和代谢物的代谢,这些物质协同作用于代谢调节系统,导致胰岛素抵抗。恢复肠道平衡的干预措施似乎具有有益的效果,可以改善血糖控制。未来的研究应该详细研究并在更大的研究中探讨其他可能的病理生理机制,以确定微生物组调节所调节的特定途径,并确定新的潜在治疗靶点。

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