Editing Vitamin B6 (section)

==Absorption, metabolism and excretion==
Vitamin B<sub>6</sub> is absorbed in the [[jejunum]] of the small intestine by [[passive diffusion]].<ref name=ODS/><ref name="DRItext"/> Even extremely large amounts are well absorbed. Absorption of the phosphate forms involves their dephosphorylation catalyzed by the enzyme [[alkaline phosphatase]].<ref name="Combs"/> Most of the vitamin is taken up by the liver. There, the dephosphorylated vitamins are converted to the phosphorylated PLP, PNP and PMP, with the two latter converted to PLP. In the liver, PLP is bound to proteins, primarily albumin. The PLP-albumin complex is what is released by the liver to circulate in plasma.<ref name="DRItext"/> Protein-binding capacity is the limiting factor for vitamin storage. Total body stores, the majority in muscle, with a lesser amount in liver, have been estimated to be in the range of 61 to 167&nbsp;mg.<ref name="DRItext"/>

Enzymatic processes utilize PLP as a phosphate-donating cofactor. PLP is restored via a [[salvage pathway]] that requires three key enzymes, [[pyridoxal kinase]], [[pyridoxine 5'-phosphate oxidase]], and [[phosphatase]]s.<ref name="Parra2018">{{cite journal |vauthors=Parra M, Stahl S, Hellmann H |title=Vitamin B<sub>6</sub> and Its Role in Cell Metabolism and Physiology |journal=Cells |volume=7 |issue=7 |date=July 2018 |page=84 |pmid=30037155 |pmc=6071262 |doi=10.3390/cells7070084 |url=|doi-access=free }}</ref><ref name="Ghatge2021"/> Inborn errors in the salvage enzymes are known to cause inadequate levels of PLP in the cell, particularly in neuronal cells. The resulting PLP deficiency is known to cause or implicated in several pathologies, most notably infant epileptic seizures.<ref name="Ghatge2021"/>

The half-life of vitamin B<sub>6</sub> varies according to different sources: one source suggests that the half-life of ''pyridoxine'' is up to 20 days,<ref name="days20">{{cite book|doi=10.1007/978-3-319-20790-2_174-1|quote=The half-life of pyridoxine is up to 20 days. |chapter=Pyridoxine |title=Critical Care Toxicology |date=2016 |last1=Kennedy |first1=Ashleigh |last2=Schaeffer |first2=Tammi |pages=1–4 |isbn=978-3-319-20790-2 }}</ref> while another source indicates half-life of ''vitamin B<sub>6</sub>'' is in range of 25 to 33 days.<ref name="VKM2017">{{cite book |title=Assessment of vitamin B<sub>6</sub> intake in relation to tolerable upper intake levels. Opinion of the Panel on Nutrition, Dietetic Products, Novel Food and Allergy of the Norwegian Scientific Committee for Food Safety |isbn=978-82-8259-260-4 |location=Oslo, Norway |url=https://vkm.no/download/18.645b840415d03a2fe8f2653d/1499330353450/087ba2170f.pdf |access-date=7 December 2019 |archive-url=https://web.archive.org/web/20191117011203/https://vkm.no/download/18.645b840415d03a2fe8f2653d/1499330353450/087ba2170f.pdf |archive-date=17 November 2019 | quote=Eighty to ninety percent of vitamin B6 in the body is found in muscles and estimated body stores in adults amount to about 170 mg with a half-life of 25-33 days.}}</ref> After considering the different sources, it can be concluded that the half-life of vitamin B<sub>6</sub> is typically measured in several weeks.<ref name="days20"/><ref name="VKM2017"/>

The end-product of vitamin B<sub>6</sub> catabolism is 4-pyridoxic acid, which makes up about half of the B<sub>6</sub> compounds in urine. 4-Pyridoxic acid is formed by the action of [[aldehyde oxidase]] in the liver. Amounts excreted increase within 1–2 weeks with vitamin supplementation and decrease as rapidly after supplementation ceases.<ref name="DRItext"/><ref name=Ueland2015 /> Other vitamin forms excreted in the urine include pyridoxal, pyridoxamine and pyridoxine, and their phosphates. When large doses of pyridoxine are given orally, the proportion of these other forms increases. A small amount of vitamin B<sub>6</sub> is also excreted in the feces. This may be a combination of unabsorbed vitamin and what was synthesized by large intestine microbiota.<ref name="DRItext"/>