There is an increasing amount of evidence that links certain disorders of the human body to an unhealthy gut microbiota (dysbiosis). This has led to increased research on gut microbes and the mechanisms involved on how they are positively or negatively affecting the host. One of the key microbes identified is Bifidobacterium bifidum due to its abundance in the human gut.
In general, BIfidobacterium species are abundant gut commensals constituting 90% of all bacteria in breast-fed infants and 4% in adults. Together with other “good” microbes present in the gut, these colonies of dense microbiota are associated with many health-promoting effects including the maintenance of the epithelial barrier function and integrity to avoid pathogen infection as well as immunomodulation. They are also known to degrade non-digestible carbohydrates and produce vitamin B, antioxidants, and linoleic acids. Among many Bifidobacterium species, B. bifidum is the most dominant species found in humans.
Our body needs help from gut bacteria to digest certain nutrients. For example, fiber-rich foods are non-digestible. B. bifidum is a prebiotic microorganism that aids in the degradation of non-digestible foods resulting in the production of a chemical called butyrate.
Butyrate, together with acetate and propionate, are short-chain fatty acids (SCFA) that are produced from microbial degradation from undigested dietary carbohydrates. Butyrate, in particular, is the least abundant among SCFA produced, but has gained attention because of its beneficial effects on both cellular energy metabolism and intestinal homeostasis. It is known to be the preferred energy source by the colonocytes with a highly efficient metabolism absorption rate which makes it undetectable in the peripheral blood.
Normally, cells undergo aerobic metabolism by using up carbohydrates (glucose) via a series of pathways starting from glycolysis, to the citric acid cycle, and the electron transport chain to convert these nutrients into energy called ATP. This whole process involves the pumping of oxygen in the mitochondria. In contrast, cancer cells undergo anaerobic metabolism due to the Warburg Effect. Essentially, the rate of nutrient (glucose) uptake in tumors and other proliferating or developing cells dramatically increases even when aerobic metabolism is possible—that is—oxygen is available and mitochondria is working. Because of this, cancer cells are heavily reliant on glucose leading to unused metabolites including butyrate.
Several studies have reported the role of butyrate in colorectal cancer. While butyrate is the preferred energy source of normal colonocytes, it is not the case for cancerous colonocytes and even inhibits the growth of the latter. Moreover, butyrate acts like that of a glycolysis inhibitor—a promising therapeutic for cancer treatment. Since cancer cells rely on glucose entering the glycolysis pathway, inhibiting this process also inhibits their energy production. With little energy to maintain themselves, energy-requiring processes stop, including their growth and proliferation.
References:
https://gut.bmj.com/content/46/4/493
https://health.clevelandclinic.org/butyrate-benefits/
https://www.cambridge.org/core/journals/nutrition-research-reviews/article/from-the-gut-to-the-peripheral-tissues-the-multiple-effects-of-butyrate/DADCCD4D5727663E689D30CDE103BBEA
https://academic.oup.com/advances/article/9/1/21/4849000
https://www.nature.com/articles/s41522-022-00312-0
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923077/
https://www.omicsonline.org/scholarly/aerobic-metabolism-journals-articles-ppts-list.php
https://www.sciencedirect.com/topics/neuroscience/glycolysis
https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/citric-acid-cycle
https://www.ncbi.nlm.nih.gov/books/NBK526105/
https://www.sciencedirect.com/topics/neuroscience/adenosine-triphosphate
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783224/
https://www.sciencedirect.com/topics/immunology-and-microbiology/anaerobic-metabolism