Biochemical and Metabolical Pathways Associated with Microbiota-Derived Butyrate in Colorectal Cancer and Omega-3 Fatty Acids Implications: A Narrative Review.

Șerban Mircea Negru,Lidia Anca Kajanto,Mădălina Preda,Elena Adriana Dumitrescu,Bogdan Georgescu,Cristian Virgil Lungulescu,Emanuel Alin Radu,Raluca Ioana Mihăilă,Dana Lucia Stănculeanu,Isabela Anda Komporaly,Adelina Silvana Gheorghe

doi:10.3390/nu14061152

Abstract

Knowledge regarding the influence of the microbial community in cancer promotion or protection has expanded even more through the study of bacterial metabolic products and how they can modulate cancer risk, which represents an extremely challenging approach for the relationship between intestinal microbiota and colorectal cancer (CRC). This review discusses research progress on the effect of bacterial dysbiosis from a metabolic point of view, particularly on the biochemical mechanisms of butyrate, one of the main short chain fatty acids (SCFAs) with anti-inflammatory and anti-tumor properties in CRC. Increased daily intake of omega-3 polyunsaturated fatty acids (PUFAs) significantly increases the density of bacteria that are known to produce butyrate. Omega-3 PUFAs have been proposed as a treatment to prevent gut microbiota dysregulation and lower the risk or progression of CRC.

Highlights

According to the estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer (GLOBOCAN) for 2020, colorectal cancer (CRC) represents one of the major health threats, especially in developed countries which are at a higher risk, due to the dietary and lifestyle patterns of the population [1,2]
The results showed that patients with CRC who received probiotics had an increased abundance of butyrate-producing bacteria in the samples from the tumor, non-tumor mucosa, and faeces, compared with the group that did not receive probiotics
The antibiotic treatment and the low-carbohydrate diet had numerous other effects observed in APCMin/+MutS homolog 2 (MSH2)−/− mice: both interventions reduced the number of cells with DNA breaks, reduced Ki-67 expression, modulated and restored the nuclear β-catenin expression to that encountered in APCMin/+MSH2+/− mice, reduced the production of numerous metabolites of microbial fermentation, decreased three butyrate-producing families within the Firmicutes phylum (Clostridiaceae, Lachnospiraceae and Ruminococcaceae) without impacting total bacterial abundance, and reduced the gene copy number for butyryl-CoA transferase [47]

Summary

Introduction

According to the estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer (GLOBOCAN) for 2020, colorectal cancer (CRC) represents one of the major health threats, especially in developed countries which are at a higher risk, due to the dietary and lifestyle patterns of the population [1,2]. It is the second leading cause of cancer death worldwide and the third most diagnosed cancer, while having a remarkable geographical variation [2,3]. Increasing data from epidemiologic, clinical, and preclinical investigations show that omega-3-PUFAs are effective in preventing CRC [10]

The Gut Microbiome and Colorectal Cancer

Microbiota-Derived Butyrate in Colorectal Cancer

Role of Omega-3 Fatty Acids in Regulating Butyrate-Producing Gut Microbiota

Conclusions and Future Perspectives