Consumption of the folate breakdown product para-aminobenzoylglutamate contributes minimally to urinary folate catabolite excretion in humans: Investigation using [13C5]para-aminobenzoylglutamate

Abstract

Folate catabolism represents the major route of folate turnover in humans and involves cleavage of the C9-N10 bond producing a pterin and para-aminobenzoylglutamate (pABG). Thus, the quantitation of pABG and its acetylated more predominant counterpart para-acetamidobenzolyglutamate (apABG) may be useful in assessing folate status and requirements. However, until the in vivo fate of dietary pABG is understood, studies using pABG excretion parameters can not be fully interpreted. As part of a larger study, an oral dose (376 nmol or 100 μg) of [13C5]pABG in 40 mL apple juice was ingested by pregnant women (2nd trimester, n = 2) and nonpregnant controls (n = 2) consuming controlled total folate intakes of 450 or 850 μg/d. Urine collections (24 h) were obtained over the next 4 d and gas chromatography-mass spectrometry was used to measure urinary [13C5]pABG, [13C5]apABG and [13C5]folate. Of the 376 nmol [13C5]pABG administered, only 17.5 ± 6.4 nmol; mean ± SEM) or 4.6 ± 1.7% of the dose was accounted for in the urine. Most of the excreted [13C5]pABG, in acetamido form (15.1 ± 5.3 nmol), was excreted the day after the dose. No urinary [13C5]folate was detected. Folate intake did not seem to influence the urinary excretion of total pABG derived from oral pABG, whereas pregnancy may lessen total pABG excretion derived from oral pABG. Overall, these results suggest that the contribution of dietary pABG to the urinary excretion of pABG and apABG is small.