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Niacin, also called nicotinic acid, functions in the body as coenzymes in the form of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinu-cleotide phosphate (NADP). These coenzymes are hydrogen acceptors; they combine with hydrogen atoms as they are removed from food substrates by many types of dehydrogenases. When a defi-ciency of niacin exists, the normal rate of dehydrogena-tion cannot be maintained; therefore, oxidative delivery of energy from the foodstuffs to the functioning ele-ments of all cells cannot occur at normal rates.
In the early stages of niacin deficiency, simple phys-iologic changes such as muscle weakness and poor glan-dular secretion may occur, but in severe niacin deficiency, actual tissue death ensues. Pathological lesions appear in many parts of the central nervous system, and permanent dementia or many types of psy-choses may result. Also, the skin develops a cracked, pigmented scaliness in areas that are exposed to mechanical irritation or sun irradiation; thus, it appears that in persons with niacin deficiency, the skin is unable to repair irritative damage.
Niacin deficiency causes intense irritation and inflammation of the mucous membranes of the mouth and other portions of the gastrointestinal tract, result-ing in many digestive abnormalities that can lead to widespread gastrointestinal hemorrhage in severe cases. It is possible that this results from generalized depres-sion of metabolism in the gastrointestinal epithelium and failure of appropriate epithelial repair.
The clinical entity called pellagra and the canine disease called black tongue are caused mainly by niacin deficiency. Pellagra is greatly exacerbated in people on a corn diet, because corn is deficient in the amino acid tryptophan, which can be converted in limited quanti-ties to niacin in the body.
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