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AJP - Endocrinology and Metabolism, Vol 272, Issue 1 E83-E85, Copyright © 1997 by American Physiological Society
ARTICLES |
D. M. Mock and G. M. Heird
Department of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children's Hospital, Little Rock 72202-3591, USA.
In human subjects, the metabolic origins of bisnorbiotin and biotin sulfoxide were determined by measuring the urinary excretion of each after chronic administration of large oral doses of biotin. For 2 wk, 14 adult volunteers consumed 1,200 micrograms of biotin per day, an amount approximately 20 times the daily dietary intake. With the use of a high-performance liquid chromatography/avidin-binding assay in untimed urine samples obtained before the first dose of biotin and after the 14th dose, concentrations of biotin, bisnorbiotin, and biotin sulfoxide were measured. Excretion was expressed as concentration ratios to urinary creatinine. Bisnorbiotin and biotin sulfoxide excretion increased 85-fold (P < 0.0001) and 114-fold (P < 0.0001), respectively. The molar percentages of bisnorbiotin and biotin sulfoxide decreased from 28 to 14% (P = 0.006) and from 9 to 5% (P = 0.017), respectively. These data provide evidence that the bisnorbiotin and biotin sulfoxide found in human urine are biotin metabolites. Furthermore, we infer that chronic consumption of large amounts of biotin does not substantially saturate the human biotin pathways of biotransformation.
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