Niacin, absorption metabolism

The absorption of niacin in the human body mainly occurs in the stomach and small intestine (Bechgaard and Jespersen 1977). Niacin is taken up by the body swiftly and quickly, and reaches peak plasma levels within 30-60 minutes of being absorbed (Bodor and Offermanns 2008). Furthermore it has a plasma half-life of 60 minutes (Carlson et al. 1968 Svedmyr and Harthon 1970). The enzyme nicotinamide adenine dinucleotide (NAD) glycohydrolase, which is found in the intestine and liver, faciUtates the synthesis of nicotinamide from NAD (Henderson and Gross 1979). This is an important step that ensures the availability of nicotinamide for the conversion to NAD. Niacin is metabolized in most tissues in the body and its metaboKtes are excreted in urine (Jacob et al. 1989 Shibata and Matsuo 1989). Importantly, niadn deficiency occurs mainly as a result of poor diet, but also other conditions such as carcinoid syndrome, Hartnup s disease and drug intake (isoniazid) (Hegyi et al. 2004). 

Several different niacin formulations are available niacin immediate-release (IR), niacin sustained-release (SR), and niacin extended-release (ER).28,29 These formulations differ in terms of dissolution and absorption rates, metabolism, efficacy, and side effects. Limitations of niacin IR and SR are flushing and hepatotoxicity, respectively. These differences appear related to the dissolution and absorption rates of niacin formulations and its subsequent metabolism. Niacin IR is available by prescription (Niacor ) as well as a dietary supplement which is not regulated by the FDA.28 Currently, there are no FDA-approved niacin SR products, thus, all SR products are available only as dietary supplements. 

The physiologically active forms of niacin are nicotinic acid, nicotinamide, and their coenzymes (93,96). Niacytin and the niacynogens appear to have limited bioavailability, although more work is needed in this area. The absorption and metabolism of niacin has been reviewed (20,93). 

Niacin (nicotinic acid pyridine-3-carboxylic acid) and nicotinamide are precursors of NAD+ and NADP+ (Figure 38-19). Niacin occurs in meat, eggs, yeast, and whole-grain cereals in conjunction with other members of the vitamin B group. Little is known about absorption, transport, and excretion of niacin and its coenzyme forms. A limited amount of niacin can be synthesized in the body from tryptophan, but it is not adequate to meet metabolic needs. 

Pellagra-like symptoms can occur in Hartnup s disease and carcinoid syndrome. Hartnup s disease is an inherited disorder of amino acid transport (Chapter 17) in which niacin deficiency presumably develops because niacin intake is inadequate to supply metabolic needs when combined with the decreased absorption of dietary tryptophan. In carcinoid syndrome, up to 60% of available dietary tryptophan is diverted to formation of 5-hydroxytryptamine (serotonin) by what is normally a minor pathway. 

This chapter discusses the pathways by which L-tryptophan is metabolized into a variety of metabolites, many of which have important physiological functions. A few metabolites are cited here briefly. Quinolinic acid is involved in the regulation of gluconeogenesis. Picolinic acid is involved in normal intestinal absorption of zinc. The body s pool of nicotinamide adenine dinucleotide (NAD) is influenced by L-tryptophan s metabolic conversion to niacin. Finally, L-tryptophan is the precursor of several neuroactive compounds, the most important of which is serotonin (5-HT), which participates as a neurochemical substrate for a variety of normal behavioral and neuroendocrine functions. Serotonin derived from L-tryptophan allows it to become involved in behavioral effects, reflecting altered central nervous system function under conditions that alter tryptophan nutrition and metabolism. 

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