The Management of Nicotinamide and Nicotinic Acid in the Mouse

Abstract

The metabolism of nicotinic acid and nicotinamide has been examined in a number of mouse tissues following intraperitoneal injection of 0.9 µmole of 14C-labeled nicotinic acid and nicotinamide. In all the tissues except liver, and to some extent intestine, nicotinamide was clearly a better precursor of DPN than was nicotinic acid. In the case of liver and intestine [14C]nicotinic acid produced a transient and considerable labeling of DPN. By 30 min after injection of nicotinic acid, label in the DPN pools of these two tissues had fallen to levels below that found after the administration of [14C]nicotinamide. The amounts of [14C]nicotinamide in the liver following [14C]nicotinic acid injection were far higher than the amounts found after injection of [14C] nicotinamide. Following the oral administration of nicotinic acid to mice, levels of nicotinic acid and nicotinamide in the blood changed in a fashion compatible with the liver and intestine serving as centers for the conversion of nicotinic acid to nicotinamide. Furthermore, it was shown that deamidation of nicotinamide to nicotinic acid was not a prerequisite for absorption of nicotinamide from the digestive tract. These observations are compatible with the hypothesis that metabolism in the mouse is designed for the utilization of nicotinamide as a precursor of DPN and that nicotinic acid is converted to nicotinamide for that purpose.