期刊
AMERICAN JOURNAL OF CLINICAL NUTRITION
卷 113, 期 1, 页码 92-103出版社
OXFORD UNIV PRESS
DOI: 10.1093/ajcn/nqaa298
关键词
alpha- or gamma-carboxyethyl hydroxychromanol (CEHC); cytochrome P450 4F2; fasting; omega-oxidation; fecal alpha-tocopherol catabolites
资金
- NIH National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [DK081761]
- Office of Dietary Supplements, ODIR, NIH
- Intramural Research Programs, NIDDK, NIH
- Metabolic Unit Staff, NIDDK Clinical Core Staff
- Clinical Center Nutrition and Nursing Department Staff, NIH
- NIDDK [DK05321311]
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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