colitis
Pathways
Studies (5)
Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation
Out of 26 patients with moderate ulcerative colitis (inflammation of the colon) who were unresponsive to conventional treatments, 92.3% responded positively and 88.5% went into remission after receiving a daily niacin enema treatment for 6 weeks. The had no serious side effects, showed notable improvements in intestinal healing, reduced symptoms like rectal bleeding and stool frequency. Niacin is a promising, well-tolerated alternative for inducing clinical remission of ulcerative colitis.
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.
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.
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.