atherosclerosis
Pathways
Studies (11)
Nicotinic Acid Treatment Shifts the Fibrinolytic Balance Favourably and Decreases Plasma Fibrinogen in Hypertriglyceridaemic Men
23 hypertriglyceridaemic men took 4g/day of niacin for 6 weeks and saw very significant improvements in lipoprotein concentrations (reducing very low density cholesterol and triglycerides by ~50%) as well as reduced blood clotting and thrombosis factors.
Leucine-nicotinic acid synergy stimulates AMPK/Sirt1 signaling and regulates lipid metabolism and lifespan in Caenorhabditis elegans, and hyperlipidemia and atherosclerosis in mice
Low dose niacin (50 mg/kg diet and 250 mg/kg diet) when supplemented in combination with leucine (24 g/kg diet) has a similar effect on lowering cholesterol in mice than standard therapeutic dose (1000 mg/kg diet) of niacin without leucine supplementation. Leucine amplifies niacin effect on lipid metabolism, hyperlipidemia and atherosclerosis in mice, at least in part by activation of the AMPK/Sirt1 axis.
Antiatherothrombotic effects of nicotinic acid
Niacin reduces blood viscosity through a variety of mechanisms, thus improving blood flow and perfusion through choke points of the vasculature. Finally, niacin has cardioprotective effects that may limit ischemia–reperfusion injury. By preserving glycolysis during periods of inadequate blood supply and improving blood flow to the heart after a stroke, niacin can improve the functional recovery of the muscular tissue of the heart.
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.
Niacin Reverses Migratory Macrophage Foam Cell Arrest Mediated by oxLDL In Vitro
Oxidized Low Density Cholesterol, oxLDL induced inhibition of macrophage migration may be reversed by Niacin, which explains part of Niacin's atheroprotective effects on cardiovascular disease independent of its effects on plasma lipids. Macrophage foam cells are a type of macrophage that localize to fatty deposits on blood vessel walls. Niacin also inhibited the formation of peroxynitrite (which is a powerful oxidant exhibiting a wide array of tissue damaging effects)
Anti-inflammatory effects of nicotinic acid
Niacin has multi-faceted anti inflammatory properties that act in both localized and systemic ways. A major area of its activity is in tissue related to fat storage via the GPR109A receptor. Dosing cells with TNF-alpha ( an inflammatory substance ) showed that niacin treated cells increased the atheroprotective hormone adiponectin and reduced macrophage chemotaxis
Anti-inflammatory effects of nicotinic acid in adipocytes demonstrated by suppression of fractalkine, RANTES, and MCP-1 and upregulation of adiponectin
Adipose tissue (body tissue used for the storage of fat) is major site of action for niacin. When adding a white blood cell attractant to adipose tissue, niacin suppresses the pro-atherogenic (plaque inducing) chemokines and upregulates the atheroprotective (protective against plaque and improves metabolism of sugar) adiponectin.
Nicotinic acid inhibits vascular inflammation via the SIRT1-dependent signaling pathway
Feeding rabbits Niacin up-regulated SIRT1 expression, which is involved with DNA repair. Rabbits where then subjected to stress via a collar on an artery in their neck and it was shown that niacin protects against blood vessel inflammation via the SIRT1/CD40-dependent signaling pathway.
Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin
9 years after the conclusion of a long term study on various drugs to reduce risk of death of people who had a heart attack, only the niacin group showed a statistically significant, 11% reduction in mortality than in the placebo group. This was after they stopped taking the niacin 9 years earlier, indicating a long term benefit.
Activated niacin receptor HCA2 inhibits chemoattractant-mediated macrophage migration via Gβγ/PKC/ERK1/2 pathway and heterologous receptor desensitization
GPR109A (aka HCA2) is highly expressed in immune cells and together with niacin seems to inhibit proinflammatory aspects of immune cell activity.
New Perspectives on the Use of Niacin in the Treatment of Lipid Disorders
An overview of research showing supplementing niacin lowers the risk of heart attack frequency and severity.