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Effect of Short-Chain Fatty Acids Produced by Probiotics
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Milena Fernandes da Silva, Meire dos Santos Falcão de Lima, Attilio Converti
There are several ways in which SCFAs protect the individual against obesity, via the activation of nutrient-specific receptors (Mulders et al. 2018). SCFAs’ affinity for the GPR41 receptor (Ffar3, free fatty acid receptor) depends on the organic acid chain length. Since the receptor GPR40, which is located near the GPR41 gene, binds to long chain fatty acids instead of SCFAs (Remely et al. 2014), it has been hypothesized that GPR41 might have no promoter region and be transcribed by the same GPR40 promoter (Bahar Halpern et al. 2012). These receptors are closely linked to the biological functions of lipid metabolism modulation, regulate the production of leptin and other hormones of satiety, and control the energy metabolism of the host (Mulders et al. 2018).
The Role of Gut Microbiota in the Pathogenesis and Treatment of Obesity
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
Stephen J. Walker, Puja B. Patel
Diets high in fiber have a favorable impact on health, indirectly by producing SCFAs through fermentation, and directly by controlling nutrient uptake, which impacts lipid and glucose metabolism. The most common SCFAs formed by gut microbiota after fiber consumption are butyrate, acetate, and propionate. They are commonly found in the large intestine, where 95% is taken in by colonocytes and utilized for energy with the following order of preference: butyrate > propionate > acetate. Most of the butyrate is used for energy by colonocytes, allowing propionate and acetate to move through the portal vein and to the liver; from there, acetate enters systemic circulation and travels to peripheral tissues. Acetate and propionate are often utilized as substrates for lipogenesis and gluconeogenesis; acetate has also been utilized for the biosynthesis of cholesterol [5]. Propionate can also be used to inhibit the synthesis of cholesterol, diminish the quantity of hepatic triglycerides, and decrease food consumption by stimulating intracellular signaling molecules, which then discharge anorexigenic peptides [40]. Many studies have investigated the association between a decrease in the availability of SCFAs to colonocytes and a variety of gut immune disorders. There has been some indirect support for this in a study examining the feces of inflammatory bowel disease patients, in which a reduction in the abundance of gut microbiota butyrate producers was found [41]. Research has also shown that butyrate can elevate internal creation of glucagon-like peptide 2 (GLP-2). The presence of GLP-2 may improve the functionality of the mucosal barrier by stimulating villus elongation and crypt cell generation, and reducing apoptosis. Butyrate has also been shown to be crucial in regulating anti-inflammatory processes through the following mechanisms: stimulating regulatory T cells to suppress inflammatory responses in the large intestine, regulating the action of macrophages of the intestine to downregulate the generation of TLR4 receptor and proinflammatory cytokines, intervening in the differentiation and maturation of monocyte-derived dendritic cells, and promoting the creation of anti-inflammatory cytokine IL-10 via binding to GPR109A receptors on intestinal macrophages and dendritic cells [5]. In mice, propionate and butyrate have shown protective effects against obesity caused by diet, as well as insulin resistance. In mice, free fatty receptors such as FFAR3 (GPR41) and FFAR2 (GPR43) are known to control how cells respond to SCFAs; however, when SCFAs stimulate GLP-1, the effect seems to be independent of FFAR3 [40]. Thus, depending on cell type, SCFA signaling through these receptors will result in a variety of functions.
The interaction between microbiome and host central nervous system: the gut-brain axis as a potential new therapeutic target in the treatment of obesity and cardiometabolic disease
Published in Expert Opinion on Therapeutic Targets, 2020
Madelief Wijdeveld, Max Nieuwdorp, Richard IJzerman
Short-chain fatty acids (SCFA) are amongst the most frequently suggested mediators of the gut microbiota-host interaction. SCFA (acetate, butyrate, and propionate) are produced by gut bacterial strains in the process of colonic fermentation of dietary fiber [23,24]. The way in which SCFA mediate the communication between gut microbiota and their host is not yet fully defined. Researchers have suggested various mechanisms of action, of which a combination presumably enables the complex interaction between gut and host. SCFA act by binding to G-protein-coupled free fatty acid receptors 2 and 3 (FFAR2 and FFAR3, i.e. GPR43 and GPR41, respectively) on enteric cells via which intestinal innervation and gut peptide secretion are mediated [25], but also exert peripheral effects after being absorbed from the gut and binding to peripheral FFAR on adipocytes, pancreatic islets, and hepatocytes [26]. Finally, there is some evidence for SCFA entering the CNS to interact with satietogenic neurons and regulatory neuropeptides [27]. With respect to their use as an energy source, butyrate is highly used by colonocytes [28] and propionate is primarily used by hepatocytes [29]. As such, only acetate is thought to reach the peripheral circulation at relatively high amounts. Locally in the gut, SCFA are able to enhance the secretion of the anorexigenic hormones GLP-1 and PYY from L cells in the gastrointestinal tract into the circulation.
Short-chain fatty acids and regulation of pancreatic endocrine secretion in mice
Published in Islets, 2019
Anne Ørgaard, Sara Lind Jepsen, Jens Juul Holst
In addition to their roles as metabolic substrates, SCFAs may also function as signaling molecules. In 2003, the free fatty acid receptors, FFAR2 (GPR43) and FFAR3 (GPR41) were deorphanized and acetate, propionate, and butyrate were identified as the predominant ligands for these receptors.10-12 FFAR2 signals through coupling to either Gαq/11, which leads to increased intracellular calcium levels via activation of phospholipase C (PLC) β, or Gαi/0, which leads to decreased cAMP production,13 whereas FFAR3 only couples to Gαi/0.14 The expression of FFAR2 and FFAR3 in various cell types in the intestinal tract is well established, and includes expression by the enteroendocrine L-cells.15-17 Several studies have indicated that SCFAs are capable of increasing the secretion of either GLP-1,15,18,19 PYY20,21 or both22,23 from L-cells, and that these effects involve binding to either FFAR2 or both FFAR2 and FFAR3.15,19,22,23 Through the secretion of GLP-1 and PYY, SCFAs have been proposed to indirectly affect host metabolism by increasing satiety and decreasing gastric emptying and gut motility.24 Furthermore, glucose stimulated insulin secretion (GSIS) from pancreatic β-cells may be affected via the stimulated secretion of GLP-1.25
Lactiplantibacillus plantarum 299v supplementation modulates β-cell ER stress and antioxidative defense pathways and prevents type 1 diabetes in gluten-free BioBreeding rats
Published in Gut Microbes, 2022
Pinar Sargin, Mark F. Roethle, Shuang Jia, Tarun Pant, Ashley E. Ciecko, Samantha N. Atkinson, Nita H. Salzman, Ru-Jeng Teng, Yi-Guang Chen, Susanne M. Cabrera, Martin J. Hessner
SCFA are recognized by the G-protein coupled receptors free fatty acid receptor 2 (FFAR2) and FFAR3. Activation of these receptors by acetate, propionate, and butyrate promote anti-inflammatory responses in innate and adaptive immune cells,38–40 while fostering Treg differentiation and activation.41 Probiotic supplementation of unaffected T1D siblings22 and metabolite-based dietary supplementation of T1D patients21 have been shown to increase circulating SCFA levels and promote greater regulatory bias in T and B cell profiles. Such analyses were not conducted here because the lymphopenia of DRlyp/lyp rats23 confounds peripheral immunophenotyping studies and comparisons to human interventions.