The interplay between diet, gut microbes, and host epigenetics in health and disease.

The interplay between diet, gut microbes, and host epigenetics in health and disease.
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饮食,肠道微生物和宿主表观遗传学在健康和疾病中的相互作用。

DOI:
10.1016/j.jnutbio.2021.108631
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发表时间:
2021-09
期刊:
The Journal of nutritional biochemistry
影响因子:
--
通讯作者:
Martinez-Guryn K
Martinez-Guryn K
中科院分区:
其他
文献类型:
--
作者:
Shock T;Badang L;Ferguson B;Martinez-Guryn K

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将微生物的功能与宿主健康联系起来的机制正在得到更好的定义,但尚未完全理解。最近探索的一种机制涉及微生物介导的宿主表观基因组的改变。特定膳食组分如纤维、硫代葡萄糖苷、多酚和膳食脂肪的消耗对肠道微生物群组成和功能具有显著影响。这些饮食成分的微生物代谢调节重要的表观遗传功能,最终影响宿主健康。饮食介导的肠道微生物组的改变调节可用于表观遗传修饰的底物,如DNA甲基化或组蛋白甲基化和/或乙酰化。此外,微生物代谢产物如丁酸盐的产生抑制核心表观遗传酶如组蛋白脱乙酰酶(HDAC)的活性。反过来,宿主表观基因组也影响肠道微生物组成。因此,这三个因素之间存在着复杂的相互作用。本文综述了饮食、肠道微生物和宿主表观遗传学在调节宿主健康方面的相互作用。具体而言,饮食对肠道微生物群结构和功能的影响,反过来又调节宿主表观遗传学,以促进对疾病发展的保护。
The mechanisms linking the function of microbes to host health are becoming better defined but are not yet fully understood. One recently explored mechanism involves microbe-mediated alterations in the host epigenome. Consumption of specific dietary components such as fiber, glucosinolates, polyphenols, and dietary fat has a significant impact on gut microbiota composition and function. Microbial metabolism of these dietary components regulates important epigenetic functions that ultimately influences host health. Diet-mediated alterations in the gut microbiome regulate the substrates available for epigenetic modifications like DNA methylation or histone methylation and/or acetylation. In addition, generation of microbial metabolites such as butyrate inhibits the activity of core epigenetic enzymes like histone deacetylases (HDACs). Reciprocally, the host epigenome also influences gut microbial composition. Thus, complex interactions exist between these three factors. This review comprehensively examines the interplay between diet, gut microbes, and host epigenetics in modulating host health. Specifically, the dietary impact on gut microbiota structure and function that in-turn regulates host epigenetics is evaluated in terms of promoting protection from disease development.
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