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首页> 外文期刊>Annals of Nutrition & Metabolism >Type 2 Diabetes and Bacteremia
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Type 2 Diabetes and Bacteremia

机译:2型糖尿病和菌血症

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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. (C) 2017 S. Karger AG, Basel
机译:背景:高比例的2型糖尿病病例与宿主遗传和环境因素有关。在过去十年中,栖息肠道的微生物被出现为肥胖症发病机制和2型糖尿病的贡献者。因此,人体肠道微生物群的操纵将为糖尿病的新治疗靶标提供必要的线索。发明内容:几项研究已经建立了2型糖尿病患者肠道脱泻病的存在,尽管这些研究中存在一些差异,但可以通过种族,饮食和方法的差异解释。肠道脱泻症会影响短链脂肪酸和二次胆汁酸的质量和数量,其充当能量,葡萄糖和脂质代谢中的信号分子。此外,肠道脱泻症会影响肠道渗透性。特别是,高脂饮食可以导致肠道微生物肿块的变化,由于紧密结蛋白的故障,例如闭塞蛋白和ZO-1 [1],强烈降低肠道渗透性。泄漏肠道的形成导致脂多糖的增加的血浆水平增加,其激活Toll样受体4并导致先天和自适应免疫应答[2]。关键消息:肠道脱虫病在肥胖症和糖尿病发病机制中起重要作用,例如,通过慢性低级炎症。正常化肠道脱泌虫病可能是一种克服胰岛素抵抗疾病的新方法,例如糖尿病。 (c)2017年S. Karger AG,巴塞尔

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