Homocysteinemia in Mice with Genetic Betaine Homocysteine S-Methyltransferase Deficiency Is Independent of Dietary Folate Intake  

Oleh:

Teng, Ya-Wen ; Cerdena, Ignacio ; Zeisel, Steven H.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 142 no. 11 (Nov. 2012), page 1964-1967.
Topik: Nutrient Physiology; Metabolism; Nutrient-Nutrient Interactions

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2012.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Elevated homocysteine (Hcy) concentrations are associated with increased risk of several chronic diseases. Hcy can be removed by methylating it to form methionine via either the betaine homocysteine S-methyltransferase (BHMT) or the methionine synthase (MS) pathway. BHMT uses betaine as the methyl donor, whereas MS uses 5-methyltetrahydrofolate. We previously found that mice with the gene encoding Bhmt deleted (Bhmt-/-) had altered Hcy metabolites in tissues. This study aimed to determine whether folate supplementation of Bhmt-/- mice reverses, and folate deficiency exacerbates, these metabolic changes. Bhmt-/- mice and their littermates (Bhmt+/+ mice) were fed a folate-deficient (FD; 0 mg/kg diet), a folate control (FC; 2 mg/kg diet), or a folate-supplemented (FS; 20 mg/kg diet) diet for 4 wk. Bhmt-/- mice had higher plasma Hcy and hepatic S-adenosylhomocysteine (AdoHcy) concentrations and had lower hepatic S-adenosylmethionine (AdoMet) concentrations compared with Bhmt+/+ mice for all diets. Although the FD diet increased plasma Hcy (P < 0.05) and hepatic AdoHcy (P < 0.001) concentrations in Bhmt+/+ mice compared with FC and FS mice, the FD diet had no effect on the metabolites measured in Bhmt-/- mice. The FS diet did not ameliorate elevated plasma Hcy and elevated hepatic AdoHcy concentrations but did increase hepatic AdoMet concentrations in Bhmt-/- mice (P < 0.001) compared with FD and FC mice. We conclude that the BHMT pathway is a major route for the elimination of Hcy in mice and that the MS pathway has little excess capacity to methylate the Hcy that accumulates when the BHMT pathway is blocked.

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