By TAP Integrative

Vitamin E supplementation, in the form of α-tocopherol, has been shown to improve liver function tests and liver histology in patients with non-alcoholic steatohepatitis (NASH)—the liver manifestation of metabolic syndrome.

The bioavailability, metabolism and status of vitamin E in patients with metabolic syndrome has been previously studied in a 2015 study published in the American Journal of Clinical Nutrition. This study demonstrated that the bioavailability of α-tocopherol was lower in patients with metabolic syndrome than in healthy adults. To follow-up on this study, researchers at Ohio State University designed a clinical trial to investigate whether urinary catabolites are useful biomarkers to evaluate vitamin E status in patients with metabolic syndrome. Results of this double-blind, crossover trial were published in 2017 by Traber and colleagues in the American Journal of Clinical Nutrition.

To understand the results of the study by Traber and colleagues requires a brief review of vitamin E metabolism. After dietary α-tocopherol is absorbed from the intestines, it enters the liver via portal circulation. The liver preferentially secretes α-tocopherol into circulation via a hepatic transfer protein. When α-tocopherol levels exceed the capacity of this transfer protein, the liver catabolizes excess α-tocopherol into α-carboxymethylbutyl hydroxychromanol (α-CMBHC) and then α-carboxyethyl hydroxychromanol (α-CEHC). Traber and colleagues hypothesized that metabolic syndrome would be associated with decreased catabolism of vitamin E and lower levels of α-CMBHC and α-CEHC in the plasma and urine.

A total of 5 healthy adults and 5 adults with metabolic syndrome ingested 15mg hexadeuterium-labeled α-tocopherol (d6-α-T) on 4 different occasions with 4 different types of milk. Plasma and urinary samples were collected during the 72-hour period following each ingestion. Baseline plasma levels of α-tocopherol were similar between groups, but when compared with healthy adults, those with metabolic syndrome excreted 30%-50% less unlabeled α-CMBHC, α-CEHC, and γ-CEHC as well as significantly less d6-α-CMBHC and d6-α-CEHC during the 24 hours after ingestion of d6-α-T. Plasma concentrations of d6-α-CEHC were also lower in patients with metabolic syndrome. Lower urinary excretion of vitamin E metabolites was associated with higher plasma c-reactive protein, interleukin-10 and interleukin-6.

Taken together, the results of this study demonstrate reduced vitamin E status in patients with metabolic syndrome and suggest that urinary vitamin E catabolites are useful biomarkers for vitamin E status.

 

Reference

Traber MG, Mah E, Leonard SW, Bobe G, Bruno RS. Metabolic syndrome increases dietary α-tocopherol requirements as assessed using urinary and plasma vitamin E catabolites: a double-blind, crossover clinical trial. Am J Clin Nutr. 2017.


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