Unless eaten in the diet, choline can only be formed during phosphatidylcholine biosynthesis through the methylation of phosphatidylethanolamine by phosphatidylethanolamine N-methyltransferase (PEMT) using S-adenosylmethionine as the methyl donor. This enzyme is most active in the liver but has been identified in many other tissues including brain and mammary gland. At least two isoforms of PEMT exist: PEMT1, localized to the endoplasmic reticulum and generating the majority of PEMT activity, and PEMT2, which resides on mitochondria-associated membranes. Both enzymes are encoded by the same gene but differ either because of post-translational modification or alternative splicing. This gene is very polymorphic and functional
SNPs (single nucleotide polymorphisms) in humans may exist and, if so, would influence dietary requirements for choline. In mice in which this gene is knocked out, the dietary requirement for choline is increased and they get fatty liver when eating a normal choline diet. Estrogen induces greater activity of PEMT perhaps explaining why premenopausal women require less choline in their diets. In addition to formation of choline, this enzyme has an essential role in lipoprotein secretion from the liver.
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