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Type-2 Diabetics Reduces Spatial Variation of Microbiome Based on Extracellur Vesicles from Gut Microbes across Human Body

机译:2型糖尿病患者可根据人体肠道微生物的细胞内囊泡减少微生物组的空间变化

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As a result of advances in sequencing technology, the role of gut microbiota in the mechanism of type-2 diabetes mellitus (T2DM) has been revealed. Studies showing wide distribution of microbiome throughout the human body, even in the blood, have motivated the investigation of the dynamics in gut microbiota across the humans. Particularly, extracellular vesicles (EVs), lipid bilayer structures secreted from the gut microbiota, have recently come into the spotlight because gut microbe-derived EVs affect glucose metabolism by inducing insulin resistance. Recently, intestine hyper-permeability linked to T2DM has also been associated with the interaction between gut microbes and leaky gut epithelium, which increases the uptake of macromolecules like lipopolysaccharide from the membranes of microbes leading to chronic inflammation. In this article, we firstly investigate the co-occurrence of stool microbes and microbe-derived EVs across serum and urine in human subjects (N?=?284), showing the dynamics and stability of gut derived EVs. Stool EVs are intermediate, while the bacterial composition in both urine and serum EVs is distinct from the stool microbiome. The co-occurrence of microbes was compared between patients with T2DM (N?=?29) and matched in healthy subjects (N?=?145). Our results showed significantly higher correlations in patients with T2DM compared to healthy subjects across stool, serum, and urine, which could be interpreted as the dysfunction of intestinal permeability in T2DM. Therefore, the significant correlation of EVs might give insight into the pathophysiological mechanisms of T2DM, as well as the role of EVs as a biomarker in the intestinal permeability of T2DM.
机译:由于测序技术的进步,揭示了肠道微生物在2型糖尿病(T2DM)的机制中的作用。甚至在血液中,均显示整个人体微生物组的广泛分布的研究促使了对人类肠道微生物群动态的调查。特别是,从肠道微生物分泌的细胞外囊泡(EVS),最近进入聚光灯,因为肠道微生物衍生的EVS通过诱导胰岛素抗性影响葡萄糖代谢。最近,与T2DM相关的肠道过渗透性也与肠道微生物和泄漏的肠道上皮之间的相互作用有关,这增加了从微生物膜等脂多糖等血清聚集的摄取导致慢性炎症。在本文中,我们首先探讨了人类受试者中血清和尿液中粪便微生物和微生物衍生的EV的共同发生(n?= 284),显示了肠道衍生EV的动态和稳定性。粪便EVS是中间体,而尿液和血清EV的细菌组合物不同于粪便微生物组。在T2DM(n = =α29)的患者之间比较微生物的共同发生,并在健康受试者中匹配(n?=Δ145)。与粪便,血清和尿液的健康受试者相比,我们的结果表明T2DM患者的相关性显着提高,这可以被解释为T2DM中肠道渗透性的功能障碍。因此,EVS的显着相关性可能对T2DM的病理生理机制以及EVS作为生物标志物的作用洞察力,以及在T2DM的肠道渗透性中的作用。

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