维生素B12
巨幼细胞性贫血
恶性贫血
生理学
医学
蛋氨酸
蛋氨酸合酶
B族维生素
贫血
内分泌学
内科学
生物化学
生物
氨基酸
作者
Luisa F. Castillo,C. Pelletier,Katarina E. Heyden,Martha S. Field
标识
DOI:10.1146/annurev-nutr-120524-043056
摘要
Folate and vitamin B 12 (B12) are essential cofactors in folate-mediated one-carbon metabolism (FOCM). FOCM includes a series of methyl transfer reactions for methionine regeneration and de novo synthesis of nucleotides, including thymidylate. Deficiency in either folate or B12 can result in negative health outcomes including megaloblastic anemia, with additional neurocognitive impairments observed as a result of B12 deficiency. While folate deficiency is not common in the United States due to mandatory folic acid fortification, B12 deficiency is observed more frequently, particularly in certain subpopulations such as vegetarians/vegans and older adults. Fortification of the food supply with folic acid has been effective to increase folate status and reduce the incidence of birth defects. However, consumption of fortified foods and use of dietary supplements containing folic acid have led to an increase in the proportion of individuals exceeding the tolerable upper intake level of folic acid. Although the interaction between folate and B12 has been appreciated for decades in relation to megaloblastic anemia, it has been recently proposed that elevated serum folate may worsen neurocognitive effects and other metabolic impairments (altered glucose homeostasis, type 2 diabetes in offspring) associated with B12 deficiency. This review highlights molecular mechanisms that may explain the biology underlying these associations with a focus on findings from studies in model systems.
科研通智能强力驱动
Strongly Powered by AbleSci AI