Utilization of niacin
Little is known about the bioavailabilitv of niacin from foods and the intraluminal factors that might affect its absorption. The mechanism for the transport of niacin across the intestinal mucosa has not been established in humans. In the rat, both the acid and amide forms of niacin are absorbed by sodium-mediated facilitated diffusion at low concen tra tions and by passive diffusion at high concentrations. Some nicotinic acid is converted to nicotinamide during passage through the mucosa. Neither form is transported against a concentration gradient.
Only nicotinic acid and nicotinamide can pass in and out of the cells of the body tissues; each cell is capable of synthesizing the coenzymes for its own use. Catabolism of tryptophan produces quinolinic acid which is then converted to NAD without formation of free nicotinamide. Nicotinamide released from the breakdown of NAD can be reused within the cell or returned to the circulation and utilized where needed. However, an appreciable amount of nicotinamide is metabolized to N1-methylnicotinamide and pyridone, which are the two major metabolites of niacin excreted in the urine. Some niacin is also excreted, but the amount is not influenced bv the intake or tissue reserves, whereas the excretion levels of the two metabolites reflect the body's niacin status and the adequacy of niacin intake. Although the urinary excretion of methylnicotinamide has been used most widely in the nutrition status surveys, the ratio of 2-pyridone to N1_ methylnicotinamide is currently considered the best available measure of niacin nutriture. On low intake the excretion of 2-pyridone declines faster than N1-methylnicotinamide and is undetectable bv the time clinical symptoms of niacin deficiency appear. The level of N1_ methylnicotinamide declines more gradually, reaching a minimum at about the time when clinical signs become evident.
