SCFA: mechanisms and functional importance in the gut

Abstract

In recent years, the importance of the gut microbiota in human health has been revealed and many publications have highlighted its role as a key component of human physiology. Owing to the use of modern sequencing approaches, the characterisation of the microbiome in healthy individuals and in disease has demonstrated a disturbance of the microbiota, or dysbiosis, associated with pathological conditions. The microbiota establishes a symbiotic crosstalk with their host: commensal microbes benefit from the nutrient-rich environment provided by the gut and the microbiota produces hundreds of proteins and metabolites that modulate key functions of the host, including nutrient processing, maintenance of energy homoeostasis and immune system development. Many bacteria-derived metabolites originate from dietary sources. Among them, an important role has been attributed to the metabolites derived from the bacterial fermentation of dietary fibres, namely SCFA linking host nutrition to intestinal homoeostasis maintenance. SCFA are important fuels for intestinal epithelial cells (IEC) and regulate IEC functions through different mechanisms to modulate their proliferation, differentiation as well as functions of subpopulations such as enteroendocrine cells, to impact gut motility and to strengthen the gut barrier functions as well as host metabolism. Recent findings show that SCFA, and in particular butyrate, also have important intestinal and immuno-modulatory functions. In this review, we discuss the mechanisms and the impact of SCFA on gut functions and host immunity and consequently on human health.

Fecal microbiota profile in patients with inflammatory bowel disease in Taiwan

“…In the present study, we identi ed that the IBD group had decrease abundance in Faecalibacterium and Subdoligranulum compared to the control group, both genera have capabilities to produce butyrate. [41] However, the concentration of butyrate or other bacterial metabolite were not exanimated in the present study.…”

“…[15,38,39] As above mentioned, butyrate belongs to SCFA and is fermented from ber-rich diets by Firmucutes, [40] including family Lachnospiraceae, Ruminococcaceae and Erysipelotrichaceae. [41] Butyrate activate target cells via G-protein-coupled receptors, and participate in the maintenance of intestinal barrier, in uence the production of proin ammatory cytokines and modulate immune response. [34,42,41,40] Reduction of butyrate and butyrate-producing bacteria probably deteriorate the disrupted mucosal barrier and uncon ned in ammation in IBD.…”

“…[41] Butyrate activate target cells via G-protein-coupled receptors, and participate in the maintenance of intestinal barrier, in uence the production of proin ammatory cytokines and modulate immune response. [34,42,41,40] Reduction of butyrate and butyrate-producing bacteria probably deteriorate the disrupted mucosal barrier and uncon ned in ammation in IBD. In the present study, we identi ed that the IBD group had decrease abundance in Faecalibacterium and Subdoligranulum compared to the control group, both genera have capabilities to produce butyrate.…”

Alteration of Colonic Mucosal Permeability during Antibiotic-Induced Dysbiosis

“…Interestingly, it has been reported that the levels of SCFAs, especially butyrate, are decreased in the cecum feces of rats treated with vancomycin [ 16 ], suggesting that a similar alteration might have occurred in our vancomycin-treated mice. SCFAs are important metabolites produced by the gut microbiome, and are capable of stimulating colonic epithelial cells via G protein-coupled receptors [ 19 ], thus likely affecting mucosal barrier function [ 20 , 21 ]. Thus, although we were unable to measure the level of SCFAs in the colon, mucosal barrier parameters such as permeability might be affected by alterations in the colonic luminal environment, including gut contents and their microbiome profile.…”

Mitochondrial Networks: A New Therapeutic Target in Colitis

“…These mechanisms play a critical role in maintaining epithelial barrier function in health and in regulating wound healing responses in the setting of colitis. 7 Inflammatory suppression of intestinal epithelial cell genes regulating butyrate transport, signaling, and mitochondrial oxidation is largely corrected by anti–tumor necrosis factor anti-inflammatory therapy. 8 However, complete healing only occurs in a minority of patients.…”