首页> 外文会议>Joint annual meeting of the International Society of Exposure Science and the International Society for Environmental Epidemiology >The Role of the Gut Microbiome on Mercury Toxicology: Protein-Rich Diet Alters Gut Microbiota Composition and Increases Methylmercury Demethylation
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The Role of the Gut Microbiome on Mercury Toxicology: Protein-Rich Diet Alters Gut Microbiota Composition and Increases Methylmercury Demethylation

机译:肠道微生物组对汞毒理学的作用:富含蛋白质的饮食改变了肠道微生物酵母组合物,增加了甲基汞去甲基化

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Methylmercury (MeHg) exposure is a global health concern particularly among coastal populations that rely on fish and marine mammals for sustenance. It has been shown that diet can modulate the MeHg kinetics and body burden. The gut microbiome has been identified as a major factor affecting contaminant metabolism, but little is known about the role of gut microbiota on mercury transformations. The objective of this study was to examine the effects of diet on the human gut microbiome and its subsequent effect on MeHg metabolism. Using a series of batch experiments, we evaluated the effects of a changing nutritional component of the diet (by altering relative abundances of carbohydrate or protein) in the gut microbial community structure of two individuals. We measured mercury methylation and demethylation rates using a stable isotope trace and conducted high throughput sequencing of the 16S rRNA metagenomic analysis to determine the microbial community structure. We observed >90% decrease in initial MeHg concentration in protein-rich diet mixed with the fecal slurry of individual A. Moreover, two microbial taxa were significantly increased from non-detectable to a total of 20% in relative proportion. Individual B gut microbiota did not exhibit similar results. A mixture of different ratios of gut microbiota of individual A and B showed similar demethylation rate as in individual A indicating that the phenotype can be conserved. Our results show that the gut microbiome of some individuals contains microbiota that can be promoted by a protein-rich diet and can increase demethylation of MeHg. The mechanism of the demethylation of MeHg needs to be characterized.
机译:甲基汞暴露尤其是依赖于鱼类和海洋哺乳动物为生沿海居民一个全球性的健康问题。它已经表明,饮食可以调节甲基汞动力学和身体负担。肠道微生物已被确定为影响污染物代谢的主要因素,但鲜为人知的是,肠道菌群对汞转化的作用。这项研究的目的是研究饮食对人体肠道微生物和甲基汞代谢及其后续效果的影响。利用一系列的一批实验中,我们评估了饮食的改变营养成分的影响(通过改变碳水化合物或蛋白质的相对丰度),在两个人的肠道微生物群落结构。我们测量汞的甲基化和使用稳定同位素示踪和的16S rRNA宏基因组分析进行高通量测序,以确定微生物群落结构去甲基化率。我们观察到> 90%的减少在初始甲基汞浓度在富含蛋白质的饮食与各个A的粪便浆料此外,二微生物类群均显著从非可检测的增加,以相对比例一个总量的20%混合。个别乙肠道菌群没有表现出类似的结果。单独的A和B的肠道菌群的不同比例的混合物显示出相似的去甲基化率如在单独的A指示的表型可以是保守的。我们的研究结果表明,一些个体的肠道微生物包含可以由富含蛋白质的饮食可以促进并能增加甲基汞的去甲基化微生物。需要被表征甲基汞的去甲基化的机理。

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