Editing Choline (section)

=== Transport ===
In humans, choline is transported as a free ion in blood. Choline–containing [[phospholipid]]s and other substances, like glycerophosphocholines, are transported in blood [[lipoprotein]]s. [[Blood plasma]] choline levels in healthy [[fasting]] adults is 7–20&nbsp;[[micromoles]] per liter (μmol/L) and 10&nbsp;μmol/L on average. Levels are regulated, but choline intake and deficiency alters these levels. Levels are elevated for about 3&nbsp;hours after choline consumption. Phosphatidylcholine levels in the plasma of fasting adults is 1.5–2.5&nbsp;mmol/L. Its consumption elevates the free choline levels for about 8–12&nbsp;hours, but does not affect phosphatidylcholine levels significantly.<ref name=eu/>

Choline is a water-soluble [[ion]] and thus requires transporters to pass through fat-soluble [[cell membrane]]s. Three types of choline transporters are known:<ref name="Inazu_2019" />
* [[SLC5A7]]
* CTLs: CTL1 ([[SLC44A1]]), CTL2 ([[SLC44A2]]) and CTL4 ([[SLC44A4]])
* OCTs: OCT1 ([[SLC22A1]]) and OCT2 ([[SLC22A2]])

SLC5A7s are [[sodium]]- (Na<sup>+</sup>) and ATP-dependent transporters.<ref name="Inazu_2019">{{cite journal | vauthors = Inazu M | title = Functional Expression of Choline Transporters in the Blood-Brain Barrier | journal = Nutrients | volume = 11 | issue = 10 | pages = 2265 | date = September 2019 | pmid = 31547050 | pmc = 6835570 | doi = 10.3390/nu11102265 | doi-access = free }}</ref><ref name=eu/> They have high [[binding affinity]] for choline, transport it primarily to [[neuron]]s and are indirectly associated with the [[acetylcholine]] production.<ref name=eu/> Their deficient function causes [[hereditary]] weakness in the pulmonary and other muscles in humans via acetylcholine deficiency. In [[knockout mice]], their dysfunction results easily in death with [[cyanosis]] and [[paralysis]].<ref>{{cite journal | vauthors = Barwick KE, Wright J, Al-Turki S, McEntagart MM, Nair A, Chioza B, Al-Memar A, Modarres H, Reilly MM, Dick KJ, Ruggiero AM, Blakely RD, Hurles ME, Crosby AH | title = Defective presynaptic choline transport underlies hereditary motor neuropathy | journal = American Journal of Human Genetics | volume = 91 | issue = 6 | pages = 1103–7 | date = December 2012 | pmid = 23141292 | pmc = 3516609 | doi = 10.1016/j.ajhg.2012.09.019 }}</ref>

CTL1s have moderate affinity for choline and transport it in almost all tissues, including the intestines, liver, kidneys, [[placenta]], and [[mitochondria]]. CTL1s supply choline for phosphatidylcholine and [[trimethylglycine]] production.<ref name=eu/> CTL2s occur especially in the mitochondria in the tongue, kidneys, muscles, and heart. They are associated with the mitochondrial [[oxidation]] of choline to trimethylglycine. CTL1s and CTL2s are not associated with the acetylcholine production, but transport choline together via the [[blood–brain barrier]]. Only CTL2s occur on the brain side of the barrier. They also remove excess choline from the neurons back to blood. CTL1s occur only on the blood side of the barrier, but also on the membranes of [[astrocyte]]s and neurons.<ref name="Inazu_2019" />

OCT1s and OCT2s are not associated with the acetylcholine production.<ref name=eu/> They transport choline with low affinity. OCT1s transport choline primarily in the liver and kidneys while  OCT2s transport choline in kidneys and the brain.<ref name="Inazu_2019" />