Metabolic Syndrome Increases Vitamin E Requirement
Key Takeaway: Researchers report that increased vitamin E supplementation may have a beneficial effect on patients with Metabolic Syndrome, as characterized by obesity, hyperlidimeia, chronic low-grade inflammation and more. The study from Ohio State University found that Metabolic Syndrome patients had decreased vitamin E catabolism, likely due to them having lower vitamin E status. Manufacturers and formulators may find value in using vitamin E-boosting custom nutrient premixes for people at risk for cardiovascular disease.
Metabolic Syndrome (MetS) is characterized by obesity, hyperlipidemia, chronic low-grade inflammation, insulin insensitivity, hyperinsulinemia, and hypertension and is a common condition among many people. MetS increases the risk of developing Type 2 diabetes1 and nonalcoholic fatty liver disease2. Nonalcoholic steatohepatitis (NASH) is common in people with MetS and is characterized by fatty infiltration into hepatocytes, inflammation, oxidative stress, and hepatic cellular injury. NASH can progress to cirrhosis, hepatocellular carcinoma, and eventually death. It is known that peroxidative damage to lipids is increased in NASH patients3, suggesting that their vitamin E requirement may be increased.
The liver plays an important role in vitamin E bioavailability. Vitamin E homeostasis is maintained by catabolism, in which the non-α-tocopherol forms of vitamin E are preferentially metabolized and the α-tocopherol form is preferentially secreted into the plasma as a function of the α-tocopherol transfer protein (α-TTP). During this process of catabolism, carboxyethyl hydroxychromanol (α-CEHC) is synthesized from its precursor α-carboxymethylbutyl hydroxychromanol (α-CMBHC) during the catabolism of vitamin E. Presumably, α-CEHC and α-CMBHC levels increase when the capacity of the liver α-TTP to secrete α-tocopherol is exceeded.
In order to determine to what extent vitamin E bioavailability may be altered by MetS, investigators from Ohio State University measured plasma and urinary concentrations of α-CEHC and α-CMBHC in 10 MetS patients and 10 healthy controls after administering a stable isotope (deuterium)-labelled dose of α-tocopherol in 4 different forms of milk in a crossover design study. The subjects consumed 5 mg α-tocopherol for 3 days before the test day and received 15 mg labeled α-tocopherol with breakfast.
The Ohio State researchers4 found that patients with MetS excreted 41% less unlabeled α-CEHC in their urine, 63% less of the labelled α-CEHC and 58% less of labelled α-CMBHC. Measuring the area under the curve (AUC) for several hours after the acute dose of 15 mg labeled vitamin E also indicated that the labeled α-CEHC breakdown product was lower (52%) in MetS patients compared to healthy controls.
The lower response to supplementation in the MetS group compared to the healthy control group indicated that the MetS patients had decreased vitamin E catabolism, which the authors speculate was due to MetS patients having lower vitamin E status than healthy controls, despite the fact that they had similar plasma α-tocopherol concentrations. The MetS patients also had higher plasma concentrations of inflammatory markers (C-reactive protein) and interleukins (IL-10 and IL-6) and blood lipids (impaired cardiometabolic health) suggesting that the lower vitamin E turnover in MetS patient may be caused by increased oxidative and inflammatory stressors. The higher circulating lipid level (hyperlipidemia) and slow vitamin E turnover are believed to be the reason that MetS patients appeared to have similar vitamin E status because their plasma vitamin E concentration was artificially elevated due to hyperlipidemia. It was also suggested that the fatty liver in MetS patients may have prevented normal hepatic α-tocopherol and α-CEHC trafficking. Alternatively, there may have been increased fecal loss of vitamin E metabolites that were not measured in this study. Regardless of the cause, the findings of this study indicate that patients with MetS have lower vitamin E status than healthy controls based on their lower excretion of both labeled and unlabeled vitamin E catabolites.
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1. Salminen M. et al Metabolic syndrome defined by modified International Federation criteria and type 2 diabetes mellitus risk: a 9-year follow-up among the aged in Finland. Diab. Vasc. Dis. Res. 2013. 10:11-16.
2. Yki-Jarvinen H. 2014. Non-alcoholic fatty liver disease as a cause and a consequence of metabolic syndrome. Lancet Diabetes Endocrinol 2:901-910.
3. Nagata K et al. 2007. Common pathogenic mechanism in development progression of liver injury caused by non-alcoholic or alcoholic steatohepatitis. J Toxicol Sci 32:453-468
4. Traber M et al Metabolic syndrome increases dietary α-tocopherol requirements as assessed using urinary and plasma vitamin E catabolites: a double-blind, crossover clinical trial. American Journal of Clinical Nutrition 2017 doi: 10.3945/ajcn.116.138495. [Epub ahead of print]