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Review
. 2024 May 29;14(6):633.
doi: 10.3390/biom14060633.

How the Western Diet Thwarts the Epigenetic Efforts of Gut Microbes in Ulcerative Colitis and Its Association with Colorectal Cancer

Avisek Majumder  1 , Shabana Bano  1
Affiliations
Review

How the Western Diet Thwarts the Epigenetic Efforts of Gut Microbes in Ulcerative Colitis and Its Association with Colorectal Cancer

Avisek Majumder et al. Biomolecules. .

Abstract

Ulcerative colitis (UC) is an autoimmune disease in which the immune system attacks the colon, leading to ulcer development, loss of colon function, and bloody diarrhea. The human gut ecosystem consists of almost 2000 different species of bacteria, forming a bioreactor fueled by dietary micronutrients to produce bioreactive compounds, which are absorbed by our body and signal to distant organs. Studies have shown that the Western diet, with fewer short-chain fatty acids (SCFAs), can alter the gut microbiome composition and cause the host's epigenetic reprogramming. Additionally, overproduction of H2S from the gut microbiome due to changes in diet patterns can further activate pro-inflammatory signaling pathways in UC. This review discusses how the Western diet affects the microbiome's function and alters the host's physiological homeostasis and susceptibility to UC. This article also covers the epidemiology, prognosis, pathophysiology, and current treatment strategies for UC, and how they are linked to colorectal cancer.

Keywords: IBS; Western diet; cancer; colorectal cancer; diet; epigenetics; gut health; hydrogen sulfide (H2S); inflammation; microbiome; short-chain fatty acids (SCFAs); therapy; ulcerative colitis (UC).

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Anatomic distribution of UC. (a) Healthy colon, and (b,c) normal anatomy of the healthy colon. Different degrees of UC: (d) proctitis, (e) proctosigmoiditis, (f) distal UC, (g) extensive UC, (h) pancolitis, and (i,j) normal anatomy of UC.
Figure 2
Figure 2
The role of food-derived SCFAs in the regulation of intestinal homeostasis: SCFAs serve as an energy substrate. In addition, they regulates various intestinal factors, like upregulating the formation of MUC-2 to maintain a healthy gut, maintaining the integrity of the tight junction, regulating Treg cells and various factors like GPR-1, GPR-4, GPR-100, and GPR-109, and activating the anti-inflammatory pathway.
Figure 3
Figure 3
On the left side, this diagram depicts the intricate relationship between environmental inputs, microorganisms, and the human host. On the right side, it shows how the gut microbiome can use undigested dietary poly- and oligosaccharides and further process them to SCFAs and other by-products (CO2, CH4, SH2, etc.); then, SCFAs can be absorbed by the human host, and other by-products can be excreted from the host’s body.
Figure 4
Figure 4
This figure schematically represents a condition of colonic inflammation via excessive H2S produced by the gut microbiota. The Western diet can increase the number of H2S-producing bacteria in the gut, and the excessive H2S produced by the microbiota can be absorbed by the colonocytes. If this absorbed H2S exceeds the H2S disposal capacity of the sulfide oxidation unit (SOU) of the colonocytes, it increases the expression of pro-inflammatory interleukin-6 and iNOS and causes an inflammatory response.
Figure 5
Figure 5
The interactions between various factors and the development of UC. Exercise, healthy food, antioxidants, and increase the production of SCFAs to maintain a healthy gut, but lack of exercise, unhealthy food, stress, excessive drugs, and decrease the production of SCFAs, which consequently leads to leaky gut or the development of UC. Triggering the immune response in UC, the main molecules involved are GPR-109, macrophage, dendritic cells, T regulatory cells, IL-6, IL-9, IL-18, and TNF-γ.
Figure 6
Figure 6
This figure schematically represents how the Western-type diet and other contributing factors cause colonic inflammation by changing the gut microbiota composition. This change can modulate the production of microbiota-produced metabolites, which then cause epigenetic changes in the host genome, thereby inducing inflammatory responses in UC.
See this image and copyright information in PMC

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References

    1. Clemente-Suárez V.J., Beltrán-Velasco A.I., Redondo-Flórez L., Martín-Rodríguez A., Tornero-Aguilera J.F. Global Impacts of Western Diet and Its Effects on Metabolism and Health: A Narrative Review. Nutrients. 2023;15:2749. doi: 10.3390/nu15122749. - DOI - PMC - PubMed
    1. Yan J., Wang L., Gu Y., Hou H., Liu T., Ding Y., Cao H. Dietary Patterns and Gut Microbiota Changes in Inflammatory Bowel Disease: Current Insights and Future Challenges. Nutrients. 2022;14:4003. doi: 10.3390/nu14194003. - DOI - PMC - PubMed
    1. Den Besten G., van Eunen K., Groen A.K., Venema K., Reijngoud D.J., Bakker B.M. The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. J. Lipid Res. 2013;54:2325–2340. doi: 10.1194/jlr.R036012. - DOI - PMC - PubMed
    1. Woo V., Alenghat T. Epigenetic regulation by gut microbiota. Gut Microbes. 2022;14:2022407. doi: 10.1080/19490976.2021.2022407. - DOI - PMC - PubMed
    1. John R.M., Rougeulle C. Developmental Epigenetics: Phenotype and the Flexible Epigenome. Front. Cell Dev. Biol. 2018;6:130. doi: 10.3389/fcell.2018.00130. - DOI - PMC - PubMed

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