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2 型糖尿病合并菌血症。

Type 2 Diabetes and Bacteremia.

机构信息

Department of Metabolism and Endocrinology, Juntendo University Graduate School of Medicine, Tokyo, Japan.

出版信息

Ann Nutr Metab. 2017;71 Suppl 1:17-22. doi: 10.1159/000479919. Epub 2017 Sep 28.

Abstract

BACKGROUND

A high proportion of type 2 diabetes cases are associated with host genetic and environmental factors. During the past decade, microorganisms that inhabit the gut have emerged as contributors to the pathogenesis of obesity and type 2 diabetes. Therefore, manipulation of the human gut microbiota will provide essential clues regarding new therapeutic targets for diabetes.

SUMMARY

Several studies have established the presence of gut dysbiosis in patients with type 2 diabetes mellitus, even though there are some differences among the studies that could be explained by differences in ethnicity, diet, and methodology. Gut dysbiosis affects the quality and quantity of short-chain fatty acids and secondary bile acids that act as signaling molecules in energy, glucose, and lipid metabolism. In addition, gut dysbiosis affect intestinal permeability. In particular, a high-fat diet can lead to changes in the gut microbiota that strongly reduce intestinal permeability due to the malfunction of tight junction proteins, such as occludin and ZO-1 [1]. The formation of leaky gut results in increased plasma levels of lipopolysaccharide, which activate Toll-like receptor 4 and result in innate and adaptive immune responses [2]. Key messages: Gut dysbiosis play an important role in the pathogenesis of obesity and diabetes, for example, via chronic low-grade inflammation. Normalizing gut dysbiosis could be a new approach to overcome diseases of insulin resistance, such as diabetes mellitus.

摘要

背景

很大比例的 2 型糖尿病病例与宿主遗传和环境因素有关。在过去的十年中,栖息在肠道内的微生物已成为肥胖和 2 型糖尿病发病机制的促成因素。因此,对人类肠道微生物群的操纵将为糖尿病的新治疗靶点提供重要线索。

摘要

尽管研究之间存在一些差异,但几项研究已经确定了 2 型糖尿病患者存在肠道菌群失调,这些差异可以通过种族、饮食和方法学的差异来解释。肠道菌群失调影响短链脂肪酸和次级胆酸的质量和数量,这些酸作为能量、葡萄糖和脂质代谢中的信号分子发挥作用。此外,肠道菌群失调还会影响肠道通透性。特别是高脂肪饮食会导致肠道微生物群发生变化,由于紧密连接蛋白(如闭合蛋白和 ZO-1)的功能障碍,肠道通透性会强烈降低[1]。渗漏肠道的形成会导致脂多糖的血浆水平升高,从而激活 Toll 样受体 4,导致先天和适应性免疫反应[2]。要点:肠道菌群失调在肥胖和糖尿病的发病机制中起重要作用,例如通过慢性低度炎症。使肠道菌群失调正常化可能是克服胰岛素抵抗疾病(如糖尿病)的一种新方法。

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