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首页> 美国卫生研究院文献>The Journal of Biological Chemistry >In Vivo Kinetics of Formate Metabolism in Folate-deficient and Folate-replete Rats
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In Vivo Kinetics of Formate Metabolism in Folate-deficient and Folate-replete Rats

机译：叶酸缺乏和叶酸充足的大鼠中甲代谢的体内动力学。

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It is now established that the mitochondrial production of formate is a major process in the endogenous generation of folate-linked one-carbon groups. We have developed an in vivo approach involving the constant infusion of [13C]formate until isotopic steady state is attained to measure the rate of endogenous formate production in rats fed on either a folate-replete or folate-deficient diet. Formate was produced at a rate of 76 μmol·h−1·100 g of body weight−1 in the folate-replete rats, and this was decreased by 44% in folate-deficient rats. This decreased formate production was confirmed in isolated rat liver mitochondria where formate production from serine, the principal precursor of one-carbon groups, was decreased by 85%, although formate production from sarcosine and dimethylglycine (choline metabolites) was significantly increased. We attribute this unexpected result to the demonstrated production of formaldehyde by sarcosine dehydrogenase and dimethylglycine dehydrogenase from their respective substrates in the absence of tetrahydrofolate and subsequent formation of formate by formaldehyde dehydrogenase. Comparison of formate production with the ingestion of dietary formate precursors (serine, glycine, tryptophan, histidine, methionine, and choline) showed that ∼75% of these precursors were converted to formate, indicating that formate is a significant, although underappreciated end product of choline and amino acid oxidation. Ingestion of a high protein diet did not result in increased production of formate, suggesting a regulation of the conversion of these precursors at the mitochondrial level to formate.
机译：现在已经确定，线粒体产生甲酸是内源性叶酸连接的一碳基团产生的主要过程。我们已经开发出一种体内方法，涉及不断注入[ 13 C]甲酸酯直到达到同位素稳定状态，以测量以叶酸充足或叶酸为食的大鼠的内源性甲酸生成速率。饮食不足。在叶酸充足的大鼠中，甲酸盐的产生速率为76μmol·h -1 ·100 g体重 -1 ，与之相比下降了44％。叶酸缺乏的大鼠。在分离的大鼠肝线粒体中证实了这种甲酸盐产量的减少，其中来自丝氨酸（一碳基团的主要前体）的甲酸盐产量减少了85％，尽管肌氨酸和二甲基甘氨酸（胆碱代谢产物）的甲酸盐产量显着增加。我们将此出乎意料的结果归因于肌氨酸脱氢酶和二甲基甘氨酸脱氢酶在不存在四氢叶酸的情况下从其各自的底物中证明产生甲醛，随后甲醛脱氢酶形成了甲酸。食用甲酸前体与食用甲酸前体（丝氨酸，甘氨酸，色氨酸，组氨酸，蛋氨酸和胆碱）的比较表明，这些前体中约有75％转化为甲酸，尽管甲酸的终产物未被充分认识，但甲酸是重要的。胆碱和氨基酸氧化。摄入高蛋白饮食不会导致甲酸盐的产生增加，这表明在线粒体水平上将这些前体转化为甲酸盐的调节。

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