Although the mechanism of the relationship between the MTHFR polymorphism and SUA is still unknown, there are several studies which assume that the MTHFR polymorphism could affect the mechanisms such as the de novo synthesis of purines via 10-formyl tetrahydrofolate with consequent overproduction of UA by the substrate of the MTHFR reaction.12,21,22) It is evident that the TT genotype of MTHFR is more closely related to the rise of plasma homocysteine in patients with a low folic acid level18,23-26) and high plasma homocysteine is lowered by folic acid fortification.27) A direct relation between plasma homocysteine levels and UA levels was also reported.12,19,28-31)
These suggest that in a group with low folic acid intake, the effects of MTHFR gene polymorphism on SUA levels are more likely to be marked, and vice versa. In this study, all of the data were collected in one healthcare center located in Shizuoka Prefecture. Shizuoka is well known for its green tea, which contains folic acid. The yearly amount of expenditure on green tea was the largest in Shizuoka, almost three times higher than the average in Japan in 2011.32) This factor could affect the results of this study.
One of the limitations of our study is the remaining unadjusted potential confounding factors associated with SUA, such as alcohol consumption, physical activity, animal protein intake, folate, and serum vitamin B12 intake, although they seemed to be independent of the MTHFR genotype. A systematic review showed that the ethnicity may affect the relationship between the MTHFR mutation and SUA levels.33)
In conclusion, though some limitations remain, the present study indicated no association between SUA and MTHFR C677T genotype among Japanese, after the influences of ABCG2 Q126X and SLC22A12 W258X were removed.
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