Niacin, absorption excretion

Absorption, Excretion and Clinical Features of Niacin Deficiency... 

Hartnup s disease. There is a defect in the epithelial transport of neutral amino acids (e.g., tryptophan) leading to poor absorption and excess excretion of these amino acids. Clinical signs resemble those of niacin deficiency (tryptophan is a precursor of niacin), namely the 3 D s Diarrhea, Dementia, Dermatitis. The condition responds to nicotinamide administration. Fan-coni s syndrome is a more generalized defect in molecular transport, involving a multitude of amino acids, glucose, calcium, phosphate, proteins, and other molecules. There may be decreased growth and rickets. 

That nongrowing animals require niacin implies that it is lost from the body either as intact niacin or as a modified or breakdown product of the vitamin. An amount of niacin equivalent to nearly 90% of our daily intake is excreted in the forms of N-methyl-2-p)nidone-5urinary metabolites can be used to assess niacin status. Loss of the normal quantity in the urine each day indicates that the supply in the diet is adequate. In humans, the healthy adult excretes 4 to 6 mg of N-methyl-nicoti-namide per day. An abnormally low level indicates that the dietary intake is not adequate. Measurement of urinary niacin metabolites has proven useful in determining the amoimt of niacin available in a variety of foods. The body s ability to use niacin in different foods may vary even if the foods contain identical quantities of the vitamin. One contributing factor to the low availability of niacin is the occurrence of the vitamin in the "bound form," as mentioned earlier. Excretion of normal levels of pyridone, for example, depends not only on normal absorption of the vitamin from the diet, but also on its conversion to NAD or NADP, followed by catabolism to the metabolite. 

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. 

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). 

Other urinary excretion products of niacin include nicotinuric acid (nicotinoyl glycine) nicotinamide N-oxide, and trigonelline (N -methyl nicotinic acid) the latter may arise from bacterial action in the gut or from the absorption of this substance from foods. The pattern of the different turnover metabolites varies between species, between diets (depending partly on the ratio of nicotinamide to nicotinic acid in the diet), and partly with niacin status thus there are complex regulatory mechanisms to be considered. 

At present, niacin status is most commonly assessed by the assay of some of the breakdown products of niacin coenzymes in the urine. Of these, -methyl nicotinamide (NMN) is the easiest to measure, because of a convenient conversion in vitro to a fluorescent product, which can then be quantitated without the need for separation. However, more definitive and reliable information can be obtained by the measurement of urinary NMN in conjunction with one or more of the urinary pyridone turnover products (N -methyl-2-pyridone-5-carboxamide and N -methyl-4-pyridone-3-carboxamide), which can be detected and quantitated by UV absorption following high-pressure liquid chromatography. The Interdepartmental Committee on Nutrition for National Defense (USA) selected the criterion of niacin deficiency in humans as an NMN excretion rate of <5.8 tmol (0.8 mg) NMN per day in 24h urine samples. 

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