| First Author | Schwahn BC | Year | 2004 |
| Journal | Metabolism | Volume | 53 |
| Issue | 5 | Pages | 594-9 |
| PubMed ID | 15131763 | Mgi Jnum | J:89359 |
| Mgi Id | MGI:3039983 | Doi | 10.1016/j.metabol.2003.10.033 |
| Citation | Schwahn BC, et al. (2004) Effects of betaine in a murine model of mild cystathionine-beta-synthase deficiency. Metabolism 53(5):594-9 |
| abstractText | Cystathionine-beta-synthase (CBS) is required for transsulfuration of homocysteine, an amino acid implicated in vascular disease. We studied homocysteine metabolism in mice with mild hyperhomocysteinemia due to a heterozygous disruption of the Cbs gene. Mice were fed diets supplemented with betaine or dimethylsulfonioacetate (DMSA); betaine and DMSA provide methyl groups for an alternate pathway of homocysteine metabolism, remethylation by betaine:homocysteine methyltransferase (BHMT). On control diets, heterozygous mice had 50% higher plasma homocysteine than did wild-type mice. Betaine and DMSA had similar effects in both genotype groups: liver betaine increased dramatically, while plasma homocysteine decreased by 40% to 50%. With increasing betaine supplementation, homocysteine decreased by 75%. Plasma homocysteine and BHMT activity both showed a strong negative correlation with liver betaine. Homocysteinemia in mice is sensitive to a disruption of Cbs and to methyl donor intake. Because betaine leads to a greater flux through BHMT and lowers homocysteine, betaine supplementation may be beneficial in mild hyperhomocysteinemia. |
