GB:肥胖相关菌群如何影响肠道表观基因组
创作:女巫 审核:szx 2018年02月06日
  • 致肥胖饮食在肥胖发生之前重塑菌群,促进产生易诱发宿主肥胖的菌群代谢产物;
  • 菌群-饮食互作可改变活性增强子的组蛋白修饰(H3K27ac和H3K4me1),这些增强子中富集了信号响应转录因子(如HNFα)的结合位点;
  • 肥胖相关的表观遗传和基因表达的变化与癌症相关信号通路有关;
  • 将肥胖小鼠菌群移植给无菌小鼠,在高脂饮食下,可诱导肥胖前期表型;
  • 宿主饮食与菌群的互作对宿主表观基因组有潜在影响,主要是宿主结肠上皮与肥胖相关的增强子。
主编推荐语
mildbreeze
这是近期在Genome Biology[IF:11.908]发表的肥胖相关的菌群研究。总体来说,饮食对菌群有强大的塑造作用,菌群-饮食的互作可“重编”肠道上皮的表观基因组,改变相关基因表达,从而影响肥胖风险。有意思的是,移植了肥胖菌群的小鼠即使吃普通食物,也表现出一定程度的血糖问题,而正常菌群则可以帮助小鼠在吃高脂食物时少长肉,再次强调肥胖和代谢问题中菌群的作用。值得关注,推荐给大家。
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Genome Biology [IF:10.806]

An obesity-associated gut microbiome reprograms the intestinal epigenome and leads to altered colonic gene expression

肥胖相关肠道菌群重新编程肠道表观基因组并改变结肠基因表达

10.1186/s13059-018-1389-1

2018-01-23, Article

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BACKGROUND: The gut microbiome, a key constituent of the colonic environment, has been implicated as an important modulator of human health. The eukaryotic epigenome is postulated to respond to environmental stimuli through alterations in chromatin features and, ultimately, gene expression. How the host mediates epigenomic responses to gut microbiota is an emerging area of interest. Here, we profile the gut microbiome and chromatin characteristics in colon epithelium from mice fed either an obesogenic or control diet, followed by an analysis of the resultant changes in gene expression.
RESULTS: The obesogenic diet shapes the microbiome prior to the development of obesity, leading to altered bacterial metabolite production which predisposes the host to obesity. This microbiota-diet interaction leads to changes in histone modification at active enhancers that are enriched for binding sites for signal responsive transcription factors. These alterations of histone methylation and acetylation are associated with signaling pathways integral to the development of colon cancer. The transplantation of obesogenic diet-conditioned microbiota into germ free mice, combined with an obesogenic diet, recapitulates the features of the long-term diet regimen. The diet/microbiome-dependent changes are reflected in both the composition of the recipient animals' microbiome as well as in the set of transcription factor motifs identified at diet-influenced enhancers.
CONCLUSIONS: These findings suggest that the gut microbiome, under specific dietary exposures, stimulates a reprogramming of the enhancer landscape in the colon, with downstream effects on transcription factors. These chromatin changes may be associated with those seen during colon cancer development.

First Authors:
Yufeng Qin

Correspondence Authors:
Paul A Wade

All Authors:
Yufeng Qin,John D Roberts,Sara A Grimm,Fred B Lih,Leesa J Deterding,Ruifang Li,Kaliopi Chrysovergis,Paul A Wade

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