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Food Science and Human Nutrition Department, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL and * U.S. Department of Agriculture, Agricultural Research Service, Western Human Nutrition Research Center, University of California-Davis, Davis, CA
3To whom correspondence should be addressed.
Folate turnover involves urinary excretion, fecal excretion, and catabolism that involves cleavage of the C9-N10 bond to yield pterins and para-aminobenzoylglutamate (pABG). Little is known about the relationship between the function of folate pools and their rates of catabolism. We report here an investigation of excretion of urinary pABG and its primary excretory form, para-acetamidobenzoylglutamate (ApABG) in samples collected during a previously published study of postmenopausal women. Ten women (4963 y) were fed a low folate diet (56 µg/d) supplemented with folic acid to yield total folate intakes of 195 µg/d (d 15), 56 µg/d (d 641), 111 µg/d (d 4269), 286 µg/d (d 7080) and 516 µg/d (d 8191). This caused changes in plasma folate, plasma homocysteine and global methylation of lymphocyte DNA. For each subject, a 7-d pooled urine sample was collected over d 17, 3642, 6470 and 8591. ApABG constituted >85% of total catabolite excretion, and folate intake did not significantly influence ApABG or pABG excretion. The molar ratio of total catabolite excretion/folate intake varied significantly, with ratios of 1.0 ± 0.17 (d 17), 3.0 ± 0.55 (d 3642), 1.1 ± 0.18 (d 6470) and 0.33 ± 0.054 (d 8591). These observations indicate that the rate of folate catabolite excretion is related mainly to masses of slow-turnover folate pools governed by long-term folate intake. Folate pools functioning in some forms of methyl group metabolism respond to dietary changes in folate intake much more rapidly.
KEY WORDS: folate catabolism para-aminobenzoylglutamate para-acetamidobenzoylglutamate humans
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