Niacin is the generic term for both nicotinic acid and nicotinamide. Niacin functions as a component of the two coenzymes (NAD) and (NADP), which are necessary for many metabolic processes, including tissue respiration, lipid metabolism, fatty acid metabolism, and glycolysis. Reduction of the coenzyme yields dihydronicotinamide (NADH or NADPH), which has a strong absorption at 340 nm, a feature widely used in assays of pyridine nucleotide-dependent enzymes.
Niacin is absorbed in the small intestine, and excess is excreted in the form of metabolites in the urine. Pellagra, the clinical syndrome resulting from niacin deficiency, is associated with diarrhea, dementia, dermatitis, and death. Niacin deficiency may result from alcoholism. To decrease lipid levels, pharmacologic doses of nicotinic acid are given therapeutically. The toxicity of niacin is low. When large doses are ingested, however, as often occurs during lipid-lowering therapies, flushing of the skin and vasodilation may occur. The RDA of niacin is 16 mg/day for adult males and 14 mg/day for an adult females. Blood or urinary niacin levels are of value in assessing niacin nutritional status.
1-Methylnicotinamide is a metabolite of nicotinamide and is produced primarily in the liver. It has anti-inflammatory properties. It is a product of nicotinamide N-methyltransferase [EC 2. 1. 1. 1] in the pathway of nicotinate and nicotinamide metabolism (KEGG). 1-Methylnicotinamide may be an endogenous activator of prostacyclin production and thus may regulate thrombotic as well as inflammatory processes in the cardiovascular system.