with doses of 3 to 4 g of niacin almost completely absorbed (Bechgaard and Jespersen, 1977). Glycohydrolases in the liver and intestines catalyze the release of nicotinamide from NAD (Henderson and Gross, 1979). Nicotinamide is then transported to tissues to be used in synthesis of NAD when needed. Both forms of the vitamin enter cells by simple diffusion; however, both nicotinic acid and nicotinamide also enter erythrocytes by facilitated transport (Lan and Henderson, 1968).

The niacin coenzymes NAD and NADP are synthesized in all tissues of the body from nicotinic acid or nicotinamide. Tissue concentrations of NAD appear to be regulated by the concentration of extracellular nicotinamide, which in turn is under hepatic control and is hormonally influenced. Hydrolysis of hepatic NAD allows the release of nicotinamide for transport to tissues that lack the ability to synthesize the NAD and NADP coenzymes from tryptophan. In the liver some excess plasma nicotinamide is converted to storage NAD (i.e., NAD not bound to enzymes). Tryptophan and nicotinic acid also contribute to storage NAD following the biosynthetic pathway, going through NAMN, which is then reamidated to NAD. In the degradation of NAD, the nicotinamide formed can be reconverted to NAD via nicotinamide ribonucleotide. Nicotinamide can be deamidated in the intestinal tract by intestinal microflora (Bernofsky, 1980).

The body’s niacin requirement is met not only by nicotinic acid and nicotinaminde present in the diet, but also by conversion from the dietary protein containing tryptophan. The relative contribution of tryptophan is estimated as follows: 60 mg of tryptophan = 1 mg of niacin = 1 mg of niacin equivalents (Horwitt et al., 1981).

Excess niacin is methylated in the liver to N¹-methyl-nicotinamide, which is excreted in the urine along with the 2- and 4-pyridone oxidation products of N¹-methyl-nicotinamide. The two major excretion products are N¹-methyl-nicotinamide and its pyridone derivative (Mrochek et al., 1976). The proportions differ somewhat depending on the amount and form of niacin ingested and the niacin status of the individual.

Pellagra is the classic manifestation of a severe niacin deficiency. It is characterized by a pigmented rash that develops symmetrically