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===Causes and mechanisms=== [[Estrogen]] production is a relevant factor which predisposes individuals to deficiency along with low dietary choline intake. Estrogens activate phosphatidylcholine producing PEMT enzymes. Women before menopause have lower dietary need for choline than men due to women's higher estrogen production. Without [[estrogen therapy]], the choline needs of post-menopausal women are similar to men's. Some [[single-nucleotide polymorphism]]s (genetic factors) affecting choline and [[folate]] metabolism are also relevant. Certain gut microbes also degrade choline more efficiently than others, so they are also relevant.<ref name="Corbin_2012" /> In deficiency, availability of phosphatidylcholines in the liver are decreased β these are needed for formation of VLDLs. Thus VLDL-mediated [[fatty acid]] transport out of the liver decreases leading to fat accumulation in the liver.<ref name=eu/> Other simultaneously occurring mechanisms explaining the observed liver damage have also been suggested. For example, choline phospholipids are also needed in [[mitochondrial]] membranes. Their unavailability leads to the inability of mitochondrial membranes to maintain proper [[electrochemical gradient]], which, among other things, is needed for degrading fatty acids via [[Ξ²-oxidation]]. Fat metabolism within the liver therefore decreases.<ref name="Corbin_2012" />
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