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Review
. 2024 Jun 29;25(13):7175.
doi: 10.3390/ijms25137175.

The Gut Microbial Regulation of Epigenetic Modification from a Metabolic Perspective

Xingtong Lin  1   2 , Hui Han  1   2 , Nan Wang  1   2 , Chengming Wang  1   2 , Ming Qi  1   2 , Jing Wang  1   2 , Gang Liu  1   3
Affiliations
Review

The Gut Microbial Regulation of Epigenetic Modification from a Metabolic Perspective

Xingtong Lin et al. Int J Mol Sci. .

Abstract

Obesity is a global health challenge that has received increasing attention in contemporary research. The gut microbiota has been implicated in the development of obesity, primarily through its involvement in regulating various host metabolic processes. Recent research suggests that epigenetic modifications may serve as crucial pathways through which the gut microbiota and its metabolites contribute to the pathogenesis of obesity and other metabolic disorders. Hence, understanding the interplay between gut microbiota and epigenetic mechanisms is crucial for elucidating the impact of obesity on the host. This review primarily focuses on the understanding of the relationship between the gut microbiota and its metabolites with epigenetic mechanisms in several obesity-related pathogenic mechanisms, including energy dysregulation, metabolic inflammation, and maternal inheritance. These findings could serve as novel therapeutic targets for probiotics, prebiotics, and fecal microbiota transplantation tools in treating metabolic disruptions. It may also aid in developing therapeutic strategies that modulate the gut microbiota, thereby regulating the metabolic characteristics of obesity.

Keywords: epigenetic modification; gut microbiota; metabolites; obesity; therapy.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
The interplay between the gut microbiota, epigenetic modifications, and obesity. The gut microbiota serves as a source of epigenetic factors, producing substrates or co-factors that modulate the epigenetic enzymes involved in energy metabolism, metabolic inflammation, and maternal inheritance-related gene epigenetic modifications, ultimately influencing the development of obesity-related diseases. HATs: histone acetyl transferases; HDAC: histone deacetylases; DNMTs: DNA methyltransferases.
See this image and copyright information in PMC

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References

    1. Devajit M., Haradhan Kumar M. Obesity and Its Related Diseases: A New Escalating Alarming in Global Health. J. Innov. Med. Res. 2023;2:12–23.
    1. Seidell J.C., Halberstadt J. The global burden of obesity and the challenges of prevention. Ann. Nutr. Metab. 2015;66((Suppl. 2)):7–12. doi: 10.1159/000375143. - DOI - PubMed
    1. Jaacks L.M., Vandevijvere S., Pan A., McGowan C.J., Wallace C., Imamura F., Mozaffarian D., Swinburn B., Ezzati M. The obesity transition: Stages of the global epidemic. Lancet Diabetes Endocrinol. 2019;7:231–240. doi: 10.1016/S2213-8587(19)30026-9. - DOI - PMC - PubMed
    1. Chong B., Jayabaskaran J., Kong G., Chan Y.H., Chin Y.H., Goh R., Kannan S., Ng C.H., Loong S., Kueh M.T.W., et al. Trends and predictions of malnutrition and obesity in 204 countries and territories: An analysis of the Global Burden of Disease Study 2019. EClinicalMedicine. 2023;57:101850. doi: 10.1016/j.eclinm.2023.101850. - DOI - PMC - PubMed
    1. Inoue Y., Qin B., Poti J., Sokol R., Gordon-Larsen P. Epidemiology of Obesity in Adults: Latest Trends. Curr. Obes. Rep. 2018;7:276–288. doi: 10.1007/s13679-018-0317-8. - DOI - PMC - PubMed