5-Methylenetetrahydrofolate reductase gene polymorphism and B-vitamins in relation to plasma homocysteine concentration and risk factors of coronary artery disease

• Main Authors: Ping-Ting, 林娉婷
• Other Authors: 黃怡嘉
• Format: Others
• Language: en_US
• Published: 2007
• Online Access: http://ndltd.ncl.edu.tw/handle/73139238035751436980

博士 === 中山醫學大學 === 營養學研究所 === 95 === The purposes of this study were to investigate B-vitamins (folate, vitamin B-6 and B-12) status, methylenetetrahydrofolate reductase (MTHFR 677C->T) gene polymorphism, homocysteine in relation to the risk of hyperlipidemia, hypertension and coronary artery disease (CAD). Furthermore, the effect of a low oral dose of folic acid on lowering the plasma homocysteine concentration in response to the MTHFR 677C->T genotypes in patients with CAD was also evaluated. Patients who were identified by cardiac catheterization as having at least 70% stenosis of one major coronary artery were assigned to the case group (n = 184). Healthy individuals with normal blood biochemical values were assigned to the control group (n = 516). MTHFR 677C->T gene polymorphism, lipid profiles, plasma homocysteine and B-vitamins concentrations were measured. Forty-six CAD patients were randomly assigned to one of two groups: a placebo group (n = 22) and a folic acid group (400ug/d folate; n = 24). Intervention was administered for 2 months (8 weeks). The results showed T-allele carriers were positively associated with blood pressure and plasma homocysteine concentration when compared to subjects with 677CC genotype. Plasma homocysteine (>= 12.5 umol/L) (OR, 3.490; 95% CI, 1.233 – 9.877) had a significant association with increased risk of CAD. However, MTHFR 677C->T genotypes had no effect on the risk of CAD. In addition, subjects with plasma PLP < 30 nmol/L exhibited higher blood lipid status and significantly increased risk of CAD (OR, 1.85; 95% CI, 1.16 – 2.95) or risk of hypertension (OR, 16.44, P < 0.001) than subjects with plasma PLP (>= 30 nmol/L. After 8 weeks of supplementation, folic acid supplements did not significantly lower fasting plasma homocysteine concentration. However, 400ug folic acid significantly reduced homocysteine by 1.8 umol/L at week 8 for those subjects with hyperhomocysteinemia, especially for subjects with the T-mutation genotype. In conclusion, T-allele carriers and low PLP (< 30 nmol/L) increased plasma homocysteine concentration, lipid profiles and blood pressure; and plasma homocysteine is associated with the risk of CAD. In addition, a low-dose folic acid supplementation (400 ug/d) may have a significant lowering effect on plasma homocysteine concentration in hyperhomocysteinemic CAD patients.