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• W2106546044 endingPage "949" @default.
• W2106546044 startingPage "946" @default.
• W2106546044 abstract "A major focus in attempts to ameliorate homocystinuria and neural tube defects is supplementation of the diet with B vitamins. The metabolic defect in these cases may be due in part to a deficiency of methyl groups. B vitamin supplementation supports the need for enzyme cofactors but cannot provide substrate in the form of methyl groups. l-Methionine is an essential amino acid and is required for protein synthesis, but it also plays a unique role in metabolism as S-adenosylmethionine, which is the primary methyl donor in metabolism. The observation that l-homocysteine, which is produced in the metabolism of l-methionine, is remethylated 2-4 times before it is destroyed is key to understanding the possibility of a methyl group deficiency. This suggests that the requirement for methyl groups (ie, S-adenosylmethionine) may be 2-4 times that for methionine in support of protein synthesis. l-Homocysteine can be remethylated to form l-methionine by betaine or N(5)-methyltetrahydrofolate. Betaine and one-carbon sources that lead to the production of N(5)-methyltetrahydrofolate and the remethylation of l-homocysteine to form l-methionine should be considered along with B vitamin supplementation in the treatment of homocystinuria and neural tube defects." @default.
• W2106546044 created "2016-06-24" @default.
• W2106546044 creator A5032265685 @default.
• W2106546044 date "2007-04-01" @default.
• W2106546044 modified "2023-09-27" @default.
• W2106546044 title "Consideration of betaine and one-carbon sources of N5-methyltetrahydrofolate for use in homocystinuria and neural tube defects" @default.
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• W2106546044 doi "https://doi.org/10.1093/ajcn/85.4.946" @default.
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