Abstract
Vitamin B12 or cobalamin is an essential nutrient with important roles in DNA synthesis, repair and methylation. It is also required in the one carbon metabolism pathway to reduce plasma homocysteine concentrations. Several epidemiological studies have indicated that genes and metabolites of the B vitamin-mediated one-carbon metabolic pathway are associated with chronic diseases. This short review describes polymorphisms in the MTHFR, FUT2 and TCN2 genes which have been implicated in cardiovascular diseases and neural tube defects amongst others.
Highlights
Vitamin B12, a water-soluble vitamin, belongs to a group of complex molecules that have cobalt containing corrin ring and are called cobalamins
Subclinical deficiencies during pregnancy have been linked with neural tube defects and in adults it has been associated with increased risk of coronary artery disease and some cancers such as colorectal cancer
Kang et al [5] first reported a more-than-threefold increase in the homozygous frequency of the Methylenetetrahydrofolate Reductase (MTHFR) polymorphism among patients with coronary artery disease, compared with controls (17% vs. 5%), and demonstrated that the elevated homocysteine levels associated with the MTHFR variant could be reduced by folic-acid administration
Summary
Vitamin B12, a water-soluble vitamin, belongs to a group of complex molecules that have cobalt containing corrin ring and are called cobalamins. Deficiencies of folate and vitamin B12 have been found to be associated with high levels of plasma homocysteine.
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