Obesity is increasingly being associated with systemic oxidative stress and inflammation. It has been noted for example that obese individuals have significantly lower plasma levels of ascorbic acid than normal weight subjects. This has been suggested to result from depletion of the antioxidant pool following increased burden of oxidative stress associated with adipose tissue accumulation. Antioxidants work in synergy and so depletion of one tends to cause increased burden upon other antioxidant systems. For example depletion of vitamin C or vitamin E leads to an increase in the ratio of oxidised glutathione to reduced glutathione. Because low levels of reduced glutathione may cause a deterioration in pancreatic β-cell function it is possible that low antioxidant status may contribute to the insulin insensitivity seen in obese individuals. In support of this, evidence suggests that vitamin E has beneficial effects on the actions of insulin.
For example, Twenty elderly subjects with normal glucose tolerance were administered either 900mg d-α-tocopherol per day or a placebo in a double blind study1. The subjects received no supplements for 4 weeks to establish a baseline before taking their treatment or placebo for 3 months. Following a 30 day wash-out period subjects then crossed over to the opposite treatment. Insulin sensitivity was assessed using a euglycaemic clamp, which is considered a reliable method. The results showed that vitamin E had a potentiating effect on whole body glucose disposal when compared to the placebo. In addition, the changes in plasma vitamin E concentrations correlated with the changes to insulin sensitivity. Vitamin E supplementation resulted in a reduction in triglyceride and free fatty acid concentrations but these changes were not correlated with changes to glucose disposal, suggesting they are mediated by different mechanisms of vitamin E.
In another study, researchers2 administered 900mg dl-α-tocopheryl acetate per day to 10 healthy control subjects and 15 subject with type 2 diabetes. Supplementation lasted for 4 months following a 4 week baseline period. Subjects then had a 1 month washout period before being switched onto the opposite treatment. In healthy subjects, vitamin E supplementation reduced the area under the curve for glucose compared to control subjects (344 versus 287mmol/L, respectively), following assessment with a euglycaemic clamp. The vitamin E supplemented subjects also experienced increased total body glucose disposal and increased non-oxidative glucose metabolism. In the diabetic subjects, vitamin E also reduced the area under the curve for glucose compared to the placebo (614 versus 544mmol/L, respectively). In addition vitamin E supplementation caused increased glucose disappearance, increased total glucose disposal and increased non-oxidative glucose metabolism.
Vitamin E therefore appears to be beneficial at increasing insulin sensitivity in both healthy and diabetic subjects. Supplementation with 900mg of vitamin E (two different forms in the two studies) was effective at raising the vitamin E levels of the subjects. In both of these studies, the increase in vitamin E concentrations in plasma was correlated with a reduction in the oxidised glutathione to reduced glutathione ration, suggesting that antioxidant capacity of tissues had been increased. In addition, the vitamin E supplementation decreased membrane microviscocity, suggesting improvements in cell permeability. The authors speculated that vitamin E decreased the burden on the glutathione system, which in turn reduced lipid peroxidation. This subsequently caused an improvement (decrease) in the membrane microviscocity improving the physical integrity of the cell which restored the glucose transport system.
RdB
