Summary: Fiber digestion produces short-chain fatty acids like propionate and butyrate, which directly alter gene expression with anti-cancer effects, according to new research. The study found that these fatty acids influence genes involved in cell proliferation, differentiation, and apoptosis, key processes that control tumor growth.
Scientists have shown these epigenetic alterations in both human cells and mouse models, emphasizing the widespread influence of fiber on health. Given that fewer than 10% of Americans adhere to recommended fiber intake levels, this research highlights the essential function of fiber in preventing cancer.
Essential Information
- Anti-Cancer Effects: Short-chain fatty acids from fiber digestion directly modulate genes that regulate cell growth, differentiation, and apoptosis.
- Global Mechanism: These fatty acids circulate throughout the body, suggesting fiber’s widespread influence on gene function.
- Diet Deficiency: Less than 10% of Americans consume the recommended daily fiber intake, limiting these protective benefits.
Source: Stanford
Fiber is well known to be an important part of a healthy diet, yet less than 10% of Americans eat the minimum recommended amount.
A recent study conducted by Stanford Medicine may finally persuade us to load our plates with fiber-rich foods such as beans, nuts, cruciferous vegetables, and avocados.
The research, which will be published in Nature Metabolism on Jan. 9 identified the direct epigenetic effects of two common byproducts of fiber digestion and found that some of the alterations in gene expression had anti-cancer actions.
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Consuming fiber leads to the production of short-chain fatty acids by the gut microbiome. These substances serve not only as an energy source for our body but have also been believed to have an indirect influence on gene activity.
The scientists investigated the effects of the two most prevalent short-chain fatty acids found in our intestines, propionate and butyrate, on gene expression in healthy human cells, as well as in both treated and untreated human colon cancer cells, and in the intestines of mice.
Researchers identified direct epigenetic modifications at certain genes involved in regulating cell growth and differentiation, as well as apoptosis, which is the process of programmed cell death. These factors are crucial for managing or interrupting the uncontrolled cell proliferation that is characteristic of cancer.
“We found a direct link between eating fiber and modulation of gene function that has anti-cancer effects, and we think this is likely a global mechanism because the short-chain fatty acids that result from fiber digestion can travel all over the body,” said Michael Snyder, PhD, Stanford W. Ascherman, MD, FACS Professor in Genetics.
"Typically, many individuals have diets that lack sufficient fiber, which results in their microbiome not receiving the proper nourishment it needs. Consequently, this limits the production of short-chain fatty acids, ultimately having a negative impact on our health."
Given the worrying rates of colon cancer in younger adults, the study findings could also spur conversation and research about the possible synergistic effects of diet and cancer treatment.
"Snyder emphasized that pinpointing the gene targets of these crucial molecules will help us comprehend how fiber delivers its positive effects and what mechanisms fail during cancer."
Updates on research concerning diet, cancer, and genetics
Author: Lisa Kim
Source: Stanford
Contact: Lisa Kim – Stanford
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Short-chain fatty acid metabolites, such as propionate and butyrate, serve as distinctive epigenetic regulators that connect dietary habits, metabolic processes, and gene expression.” by Michael Snyder et al. Nature Metabolism
Summary
Short-chain fatty acid metabolites, such as propionate and butyrate, serve as distinctive epigenetic regulators that connect dietary habits, metabolic processes, and gene expression.
Short-chain fatty acids (SCFAs) such as propionate and butyrate offer various health benefits, are produced abundantly through microbial metabolism, and have been recognized as distinctive acyl lysine histone modifications.
In order to gain deeper insights into the role of these modifications, we employed chromatin immunoprecipitation coupled with sequencing to delineate the genome-wide distribution of four short-chain acyl histone marks: H3K18pr, H3K18bu, H4K12pr, and H4K12bu. This analysis was conducted on both treated and untreated colorectal cancer (CRC) cells, normal cells, and mouse intestines in vivo.
We analyze the relationship between these marks and open chromatin regions, along with gene expression, to evaluate the functionality of the target areas. Our findings reveal that propionate and butyrate interact with and promote the expression of genes that play roles in growth, differentiation, and ion transport.
We suggest a process in which short-chain fatty acids (SCFAs) directly alter particular genomic areas, leading to enhanced chromatin accessibility. Notably, butyrate exhibits contrasting impacts on the growth of normal cells compared to colorectal cancer (CRC) cells.
