Niacin, also known as nicotinic acid, is a derivative of pyridine that is substituted. Nicotinamide adenine dinucleotide (NAD+) and its phosphorylated form, nicotinamide adenine dinucleotide phosphate (NADP+), are the biologically active coenzyme forms, as shown in Figure 28.13. Nicotinamide, which is derived from nicotinic acid and contains an amide group instead of a carboxyl group, is also present in the diet. Nicotinamide is easily deaminated in the body, making it nutritionally equivalent to nicotinic acid. NAD+ and NADP+ function as coenzymes in oxidation-reduction reactions, in which the coenzyme accepts two electrons from a hydride ion, resulting in the reduction of the pyridine ring, as illustrated in Figure 28.14. The reduced forms of NAD+ and NADP+ are NADH and NADPH, respectively. It is worth noting that quinolinate, a metabolite of tryptophan, can be converted into NAD(P). Additionally, it is important to recognize that 1 mg of niacin is equivalent to 60 mg of tryptophan. The distribution of niacin can be found in unrefined and enriched grains and cereals, milk, and lean meats, particularly liver.

When it comes to clinical indications for niacin, there are two main aspects to consider. Firstly, niacin deficiency leads to pellagra, a condition that affects the skin, gastrointestinal tract, and central nervous system. Pellagra symptoms progress through three Ds: dermatitis (photosensitive), diarrhea, and dementia. If left untreated, it can result in death (the fourth D). Additionally, a pellagra-like condition can arise due to Hartnup disorder, which involves faulty absorption of tryptophan. Corn-based diets, which are low in niacin and tryptophan, can also contribute to pellagra. Secondly, niacin is employed in the treatment of hyperlipidemia. At doses of 1.5 g/day, or 100 times the recommended dietary allowance (RDA), niacin significantly inhibits lipolysis in adipose tissue, which is the primary source of circulating free fatty acids (FFA). Normally, the liver utilizes these circulating FFA as a major precursor for synthesizing triacylglycerol (TAG). Consequently, niacin reduces TAG synthesis in the liver, which is necessary for producing very-low-density lipoprotein (VLDL). In the plasma, low-density lipoprotein (LDL), the lipoprotein rich in cholesterol, is derived from VLDL. Thus, both plasma TAG (found in VLDL) and cholesterol (found in LDL) are lowered by niacin. As a result, niacin is particularly effective in treating type IIb hyperlipoproteinemia, a condition characterized by elevated levels of both VLDL and LDL. However, it is important to note that high doses of niacin can cause acute flushing mediated by prostaglandins. The use of aspirin can mitigate this side effect by inhibiting prostaglandin synthesis. Itching may also occur. Additionally, niacin increases levels of high-density lipoprotein and lowers levels of Lp(a). Moving on to riboflavin (vitamin B2)...
Niacin, or nicotinic acid, is a substituted pyridine derivative. The biologically active coenzyme forms are nicotinamide adenine dinucleotide (NAD+) and its phosphorylated derivative, nicotinamide adenine dinucleotide phosphate (NADP+), as shown in Figure 28.13. Nicotinamide, a derivative of nicotinic acid that contains an amide instead of a carboxyl group, also occurs in the diet. Nicotinamide is readily deaminated in the body and, therefore, is nutritionally equivalent to nicotinic acid. NAD+ and NADP+ serve as coenzymes in oxidation–reduction reactions in which the coenzyme undergoes reduction of the pyridine ring by accepting two electrons from a hydride ion, as shown in Figure 28.14. The reduced forms of NAD+ and NADP+ are NADH and NADPH, respectively. [Note: A metabolite of tryptophan, quinolinate, can be converted to NAD(P). In comparison, 60 mg of tryptophan = 1 mg of niacin.] to NADH. [Note: The hydride ion consists of a hydrogen (H) atom plus an electron.] = phosphate.
A. Distribution
Niacin is found in unrefined and enriched grains and cereal, milk, and lean meats (especially liver).
B. Clinical indications for niacin 1.
Deficiency: A deficiency of niacin causes pellagra, a disease involving the skin, gastrointestinal tract, and CNS. The symptoms of pellagra progress through the three Ds: dermatitis (photosensitive), diarrhea, and dementia. If untreated, death (a fourth D) occurs. Hartnup disorder, characterized by defective absorption of tryptophan, can result in pellagra-like symptoms. [Note: Corn is low in both niacin and tryptophan. Corn-based diets can cause pellagra.] 2.
Hyperlipidemia treatment: Niacin at doses of 1.5 g/day, or 100 times the RDA, strongly inhibits lipolysis in adipose tissue, the primary producer of circulating free fatty acids (FFA). The liver normally uses these circulating FFA as a major precursor for triacylglycerol (TAG) synthesis. Thus, niacin causes a decrease in liver TAG synthesis, which is required for very-low-density lipoprotein ([VLDL] see p. 230) production. Low-density lipoprotein (LDL, the cholesterol-rich lipoprotein) is derived from VLDL in the plasma. Thus, both plasma TAG (in VLDL) and cholesterol (in LDL) are lowered. Therefore, niacin is particularly useful in the treatment of type IIb hyperlipoproteinemia, in which both VLDL and LDL are elevated. The high doses of niacin required can cause acute, prostaglandin-mediated flushing. Aspirin can reduce this side effect by inhibiting prostaglandin synthesis (see p. 214). Itching may also occur. [Note: Niacin raises high-density lipoprotein and lowers Lp(a) levels (see p. 237).]
VIII. RIBOFLAVIN (VITAMIN B2)