Summary: Fiber fermentation produces short-chain fatty acids like propionate and butyrate, which immediately alter gene expression with anti-cancer results, according to new research. The research found that these fatty acids affect genes involved in cell proliferation, distinction, and death, important processes that control cyst growth.
These genetic changes were demonstrated by researchers in mouse and human cell models, highlighting the health impact of fiber. With less than 10 % of Americans meeting grain intake instructions, this study underscores fiber’s important role in cancer prevention.
Essential Information
- Anti-Cancer Effects: Short-chain fatty acid from fibers digestion directly modulate chromosomes that control body growth, differentiation, and death.
- International System: These fatty acids circulate throughout the system, suggesting fiber’s common effect on gene functionality.
- Diet Deficiency: Less than 10 % of Americans consume the recommended daily fiber diet, limiting these defensive benefits.
Origin: Stanford
Fiber is well known to be an important part of a healthy diet, but  , less than 10 % of Americans , eat the minimum recommended amount.
A new research from Stanford Medicine may eventually urge us to fill our plates with beans, nuts, other vegetables, avocados and another fiber-rich foods.
The study, which will be published in , Nature Metabolism , on Jan. 9 identified the strong genetic effects of two popular byproducts of grain digestion and found that some of the alterations in dna expression had anti-cancer actions.
When we eat grain, the gut bacteria produces short-chain fatty acid. These substances have long been thought to have an indirect impact on protein work, making them more than just a source of energy for us.
The experts traced how the two most common short-chain fatty acid in our gut, propionate and butyrate, altered gene expression in wholesome human tissue, in treated and untreated people colon cancer tissue, and in keyboard intestines.
They discovered direct epigenetic changes at specific genes that control cell proliferation and differentiation, as well as apoptosis and pre-programmed cell death processes, all of which are crucial for preventing or halting the unchecked cell growth that underlies 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.
” People’s diets typically contain a lot of fiber, which means that their microbiome is not getting enough of it and isn’t producing as many short-chain fatty acids as it should.” This is bad for our health in any way.
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 continued,” We can better understand how fiber exerts its beneficial effects and what goes wrong during cancer by identifying the gene targets of these crucial molecules.”
About this diet, cancer, and genetics research news
Author: Lisa Kim
Origin: Stanford
Contact: Lisa Kim – Stanford
Image: The image is credited to Neuroscience News
Original Research: Open access.
The authors, Michael Snyder and al., have developed a unique epigenetic regulatory framework that links diet, metabolism, and gene expression. Nature Metabolism
Abstract
Propionate and butyrate are two distinct epigenetic regulatory molecules that link diet, metabolism, and gene expression.
The acyl lysine histone marks (SCFAs ) propionate and butyrate, which are produced in large quantities by microbial metabolism, have been identified as unique acyl lysine marks (SCFAs ).
To better understand the function of these modifications, we used chromatin immunoprecipitation followed by sequencing to map the genome-wide location of four short-chain acyl histone marks, H3K18pr, H3K18bu, H4K12pr and H4K12bu, in treated and untreated colorectal cancer ( CRC ) and normal cells as well as in mouse intestines in vivo.
To learn the function of the target regions, we correlate these marks with open chromatin regions and gene expression. Our research demonstrates that propionate and butyrate bind and serve as promoters of genes involved in ion transport, differentiation, and growth.
We develop a mechanism that involves SCFA direct modification of specific genomic regions, which leads to increased chromatin accessibility and, in the case of butyrate, opposing effects on the proliferation of CRC and normal cells.
