butyrate
Pathways
Studies (10)
Effect of Different Levels of Niacin on Serum Biochemical Parameters, Antioxidant Status, Cytokine Levels, Inflammatory Gene Expression and Colonic Microbial Composition in Weaned Piglets
Piglets separated from their mother in agriculture tend to struggle health wise. Supplementing their diet with niacin significantly improves their survivability via factors like improved colonic microbial diversity, intestinal health, reduced intestinal inflammation and improved overall immunity.
Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis
Niacin, a pharmacological Gpr109a agonist, suppressed colitis and colon cancer in a Gpr109a-dependent manner in mice. Thus, Gpr10a has an essential role in mediating the beneficial effects of gut microbiota and dietary fiber in colon.
Intestinal Flora as a Potential Strategy to Fight SARS-CoV-2 Infection
Many microbial metabolites, especially butyrate, found in the intestinal flora, are extremely important in regulating systemic and pulmonary immune and inflammatory responses and have a wide range of anti-inflammatory and immunity enhancing functions. Improving intestinal micro-ecology via like butyrate supplementation may partially mediate the effects of SARS-CoV-2 on the both local gastrointestinal response and systemic immune response of the host, and thus be a target for COVID-19 prevention and treatment.
Deficient butyrate-producing capacity in the gut microbiome of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome patients is associated with fatigue symptoms
People with Myalgic Encephalomyelitis / Chronic Fatigue Syndrome have a deficit in the butyrate-producing capacity of the gut microbiome. The relationships observed among symptom severity and gut microbiome disturbances suggests a causal linkage and support research into interventions that boost butyrate production.
Activation of Gpr109a, Receptor for Niacin and the Commensal Metabolite Butyrate, Suppresses Colonic Inflammation and Carcinogenesis
GPR109A expressed in immune cells as well as in colonic tissue is necessary for protection against colitis and colon carcinogenesis. Niacin suppresses colitis and colon cancer in a GPR109A-dependent manner. GPR109A is key in mediating the beneficial effects of gut microbiota and dietary fiber in colon. Niacin suppresses atherosclerosis by activating GPR109A in immune cells. GPR109A mediates butyrate effects in colon and is a critical molecular link between colonic bacteria and dietary fiber and the host.
Gut dysbiosis dysregulates central and systemic homeostasis via decreased melatonin and suboptimal mitochondria functioning: pathoetiological and pathophysiological implications.
In depth review of how deficiency of butyrate and melatonin compromise gut and overall mitochondrial function and lead to lower levels of other key molecules in cellular metabolism like sirtuins, PGC-1α and NAD+.
Decreased expression of G-protein-coupled receptors GPR43 and GPR109a in psoriatic skin can be restored by topical application of sodium butyrate
Psoriatic skin has reduced GPR109A expression, topical sodium butyrate increases GPR109A expression in skin and is potentially useful in psoriasis therapy.
The Niacin/Butyrate Receptor GPR109A Suppresses Mammary Tumorigenesis by Inhibiting Cell Survival
The expression of niacin receptor GPR109A is decreased by over 70% in breast cancer samples. It's reduced in early stages, and almost undetectable in advanced stages. Increasing expression of GPR109A seems to act as a tumor suppressor in breast tissue, but interestingly can also acts as tumor protective in other tissues like skin, mechanism of differentiation unknown.
Melatonin alleviates titanium nanoparticles induced osteolysis via activation of butyrate/GPR109A signaling pathway
Supplementing mice with melatonin increases butyrate production in their gut via bacteria, conversely antibiotics severely impair this butyrate production. When mice are poisoned with titanium nanoparticles to induce bone deterioration, butyrate has a protective effect against bone loss. This protective effect is specifically dependent on the GPR109A receptor that seems to be activated by the butyrate enriched gut microbiota.
Activation of the receptor (Gpr109a) for niacin and the commensal metabolite butyrate suppresses colonic inflammation and carcinogenesis
GPR109A plays an essential role in gut health. GPR109A deficiency worsens colitis and colonic inflammation in mice. GPR109A expression is necessary for immune health. Antibiotics mess up butyrate producing gut bacteria, thus reducing GPR109A.