Samenvatting
The gut microbiota represents a metabolically active biomass of up to 2 kg in adult humans. Microbiota-derived molecules significantly contribute to the host metabolism. Large amounts of bacterial metabolites are taken up by the host and are subsequently utilized by the human body. For instance, short chain fatty acids produced by the gut microbiota are a major energy source of humans.
It is widely accepted that microbiota-derived metabolites are used as fuel for beta-oxidation (short chain fatty acids) and participate in many metabolic processes (vitamins, such as folic acid). Apart from these direct metabolic effects, it also becomes more and more evident that these metabolites can interact with the mammalian epigenetic machinery. By interacting with histones and DNA they may be able to manipulate the host's chromatin state and functionality and hence its physiology and health.
In this chapter, we summarize the current knowledge on possible interactions of different bacterial metabolites with the mammalian epigenetic machinery, mostly based on in vitro data. We discuss the putative impact on chromatin marks, for example histone modifications and DNA methylation. Subsequently, we speculate about possible beneficial and adverse consequences for the epigenome, the physiology and health of the host, as well as plausible future applications of this knowledge for in vivo translation to support personal health.
Originele taal-2 | English |
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Titel | MICROBIOTA OF THE HUMAN BODY: IMPLICATIONS IN HEALTH AND DISEASE |
Subtitel | Implications in Health and Disease |
Redacteuren | Andreas Schwiertz |
Uitgeverij | SPRINGER INT PUBLISHING AG |
Pagina's | 33-44 |
Aantal pagina's | 12 |
Volume | 902 |
ISBN van elektronische versie | 978-3-319-31248-4 |
ISBN van geprinte versie | 978-3-319-31246-0 |
DOI's | |
Status | Published - 2016 |
Publicatie series
Naam | Advances in Experimental Medicine and Biology |
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Uitgeverij | Springer International Publishing |
Volume | 902 |
ISSN van geprinte versie | 0065-2598 |
ISSN van elektronische versie | 0065-2598 |