Editing Galactose (section)

==Metabolism==
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[[File:Leloir pathway.png|300px|thumb|right|Galactose metabolism]]
Glucose is more stable than galactose and is less susceptible to the formation of nonspecific glycoconjugates, molecules with at least one sugar attached to a protein or lipid. Many speculate that it is for this reason that a pathway for rapid conversion from galactose to glucose has been [[Conserved sequence|highly conserved]] among many species.<ref name=OMMBID72>{{cite book |chapter-url=https://ommbid.mhmedical.com/content.aspx?bookid=971&sectionid=62672411 |chapter-url-access=subscription |title=The Online Metabolic and Molecular Bases of Inherited Disease |chapter=Galactosemia |vauthors=Fridovich-Keil JL, Walter JH |veditors=Valle D, Beaudet AL, Vogelstein B, Kinzler KW, Antonarakis SE, Ballabio A, Gibson KM, Mitchell G |access-date=2018-06-25 |archive-date=2018-06-26 |archive-url=https://web.archive.org/web/20180626030220/https://ommbid.mhmedical.com/content.aspx?bookid=971&sectionid=62672411 |url-status=dead }}<br />a 4 b 21 c 22 d 22</ref>

The main pathway of galactose metabolism is the [[Leloir pathway]]; humans and other species, however, have been noted to contain several alternate pathways, such as the [[De Ley Doudoroff Pathway]]. The Leloir pathway consists of the latter stage of a two-part process that converts β-D-galactose to [[Uridine diphosphate glucose|UDP-glucose]]. The initial stage is the conversion of β-D-galactose to α-D-galactose by the enzyme, mutarotase (GALM). The Leloir pathway then carries out the conversion of α-D-galactose to UDP-glucose via three principal enzymes: Galactokinase (GALK) phosphorylates α-D-galactose to galactose-1-phosphate, or Gal-1-P; Galactose-1-phosphate uridyltransferase (GALT) transfers a UMP group from UDP-glucose to Gal-1-P to form UDP-galactose; and finally, UDP galactose-4’-epimerase (GALE) interconverts UDP-galactose and UDP-glucose, thereby completing the pathway.<ref name=Bosch07>{{cite journal | vauthors = Bosch AM | title = Classical galactosaemia revisited | journal = Journal of Inherited Metabolic Disease | volume = 29 | issue = 4 | pages = 516–25 | date = August 2006 | pmid = 16838075 | doi = 10.1007/s10545-006-0382-0 | s2cid = 16382462 }}<br /> a 517 b 516 c 519</ref>

The above mechanisms for galactose metabolism are necessary because the human body cannot directly convert galactose into energy, and must first go through one of these processes in order to utilize the sugar.<ref>{{Cite book|last1=Berg|first1=Jeremy M.|last2=Tymoczko|first2=John L.|last3=Stryer|first3=Lubert|date=2013|title=Stryer Biochemie|url=http://dx.doi.org/10.1007/978-3-8274-2989-6|doi=10.1007/978-3-8274-2989-6|isbn=978-3-8274-2988-9}}</ref>

[[Galactosemia]] is an inability to properly break down galactose due to a genetically inherited mutation in one of the enzymes in the Leloir pathway. As a result, the consumption of even small quantities is harmful to galactosemics.<ref>{{cite journal|url=https://www.ncbi.nlm.nih.gov/books/NBK1518|title=Classic Galactosemia and Clinical Variant Galactosemia| first = Gerard T | last = Berry | name-list-style = vanc |journal=Nih.gov|access-date=17 May 2015|publisher=University of Washington, Seattle|year=1993|pmid=20301691}}</ref>