4.7 Article

Vitamin E catabolism in women, as modulated by food and by fat, studied using 2 deuterium-labeled α-tocopherols in a 3-phase, nonrandomized crossover study

Journal

AMERICAN JOURNAL OF CLINICAL NUTRITION
Volume 113, Issue 1, Pages 92-103

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/ajcn/nqaa298

Keywords

alpha- or gamma-carboxyethyl hydroxychromanol (CEHC); cytochrome P450 4F2; fasting; omega-oxidation; fecal alpha-tocopherol catabolites

Funding

  1. NIH National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [DK081761]
  2. Office of Dietary Supplements, ODIR, NIH
  3. Intramural Research Programs, NIDDK, NIH
  4. Metabolic Unit Staff, NIDDK Clinical Core Staff
  5. Clinical Center Nutrition and Nursing Department Staff, NIH
  6. NIDDK [DK05321311]

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The study investigated the roles of the intestine and liver in alpha-tocopherol catabolism under conditions of fat or fasting, revealing differential catabolism of intravenous d(6)-alpha-tocopherol and oral d(3)-alpha-tocopherol. This suggests that both liver and intestine play a role in the metabolism of alpha-tocopherol, with variations in catabolite excretion observed between different interventions.
Background: Human vitamin E (alpha-tocopherol) catabolism is a mechanism for regulating whole-body alpha-tocopherol. Objectives: To determine the roles of the intestine and liver on alpha-tocopherol catabolism as affected by fat or fasting, 2 deuteriumlabeled (intravenous d(6)- and oral d(3)-) forms of alpha-tocopherol were used. Methods: Healthy women received intravenous d(6)-alpha-tocopherol and consumed d(3)-alpha-tocopherol with a 600-kcal defined liquid meal (DLM; 40% or 0% fat, n = 10) followed by controlled meals; or the 0% fat DLM (n = 7) followed by a 12-h fast (0% fat-fast), then controlled meals <= 72 h. The order of the 3-phase crossover design was not randomized and there was no blinding. Samples were analyzed by LC/MS to determine the alpha-tocopherol catabolites and alpha-carboxyethyl hydroxychromanol (alpha-CEHC) in urine, feces, and plasma that were catabolized from administered oral d3- and intravenous d(6)-alpha-tocopherols. Results: Urinary and plasma d(3)- and d(6)-alpha-CEHC concentrations varied differently with the interventions. Mean +/- SEM cumulative urinary d(6)-alpha-CEHC derived from the intravenous dose excreted over 72 h during the 40% fat (2.50 +/- 0.37 mu mol/g creatinine) and 0% fat (2.37 +/- 0.37 mu mol/g creatinine) interventions were similar, but a similar to 50% decrease was observed during the 0% fat-fast (1.05 +/- 0.39 mu mol/g creatinine) intervention (compared with 0% fat, P = 0.0005). Cumulative urinary d(3)-alpha-CEHC excretion was not significantly changed by any intervention. Total urinary and fecal excretion of catabolites accounted for <5% of each of the administered doses. Conclusions: Differential catabolism of the intravenous d(6)-atocopherol and oral d(3)-alpha-tocopherol doses shows both liver and intestine have roles in alpha-tocopherol catabolism. During the 40% fat intervention, >90% of urinary d(3)-alpha-CEHC excretion was estimated to be liver-derived, whereas during fasting <50% was from the liver with the remainder from the intestine, suggesting that there was increased intestinal alpha-tocopherol catabolism while d(3)-alpha-tocopherol was retained in the intestine in the absence of adequate fat/food for alpha-tocopherol absorption.

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