Editing Niacin (section)

===Pharmacokinetics===
Both nicotinic acid and nicotinamide are rapidly absorbed from the stomach and small intestine.<ref>{{cite journal | vauthors = Said HM | title = Intestinal absorption of water-soluble vitamins in health and disease | journal = The Biochemical Journal | volume = 437 | issue = 3 | pages = 357–372 | date = August 2011 | pmid = 21749321 | pmc = 4049159 | doi = 10.1042/BJ20110326 }}</ref> Absorption is facilitated by sodium-dependent diffusion, and at higher intakes, via passive diffusion. Unlike some other vitamins, the percent absorbed does not decrease with increasing dose, so that even at amounts of 3-4 grams, absorption is nearly complete.<ref name=PKIN2020Niacin /> With a one gram dose, peak plasma concentrations of 15 to 30 μg/mL are reached within 30 to 60 minutes. Approximately 88% of an oral pharmacologic dose is eliminated by the kidneys as unchanged niacin or nicotinuric acid, its primary metabolite. The plasma elimination half-life of niacin ranges from 20 to 45 minutes.<ref name=DailyMed />

Niacin and nicotinamide are both converted into the [[coenzyme]] NAD.<ref name="isbn1-57259-153-6">{{cite book | vauthors = Cox M, Lehninger AL, Nelson DR | title = Lehninger principles of biochemistry | publisher = Worth Publishers | location = New York | year = 2000 | isbn = 978-1-57259-153-0 | url-access = registration | url = https://archive.org/details/lehningerprincip01lehn }}</ref> NAD converts to NADP by phosphorylation in the presence of the enzyme [[NAD+ kinase]].  High energy requirements (brain) or high turnover rate (gut, skin) organs are usually the most susceptible to their deficiency.<ref>{{cite journal | vauthors = Ishii N, Nishihara Y | title = Pellagra among chronic alcoholics: clinical and pathological study of 20 necropsy cases | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 44 | issue = 3 | pages = 209–15 | date = March 1981 | pmid = 7229643 | pmc = 490893 | doi = 10.1136/jnnp.44.3.209 }}</ref> In the liver, nicotinamide is converted to storage [[nicotinamide adenine dinucleotide]] (NAD). As needed, liver NAD is hydrolyzed to nicotinamide and niacin for transport to tissues, there reconverted to NAD to serve as an enzyme cofactor.<ref name=PKIN2020Niacin /> Excess niacin is methylated in the liver to N<sup>1</sup>-methylnicotinamide (NMN) and excreted in urine as such or as the oxidized metabolites [[N1-Methyl-2-pyridone-5-carboxamide|N<sup>1</sup>-methyl-2-pyridone-5-carboxamide]] and [[N1-Methyl-4-pyridone-3-carboxamide]] (2PY and 4PY). Decreased urinary content of these metabolites is a measure of niacin deficiency.<ref name=PKIN2020Niacin />