Obesity is increasingly being seen a condition that is associated with inflammation and oxidative stress. In turn, oxidative stress is implicated in the complications of type 2 diabetes. This association is highlighted in research that shows that plasma vitamin C levels are inversely associated with obesity. High doses of vitamin C and vitamin E are known to increase reduced glutathione (GSH) in plasma because these antioxidants are able to preserve glutathione by causing increased recycling of the oxidised forms of glutathione (GSSG) to the reduced form, and this removes the burden of oxidative stress from the glutathione system. It has been shown that increasing the ratio of oxidised to reduced glutathione in plasma may affect the response of the β-cells of the pancreas to glucose. This effects has been demonstrated in research that reported reduced oxidative stress and improved insulin action upon administration of large doses of vitamin E in humans.
For example, researchers1 administered either 900 mg per day vitamin E or a placebo to ten healthy and fifteen type 2 diabetics for four months to assess the effects of supplementation on insulin levels. The insulin resistance and glucose disposal of the subjects were tested prior to supplementation using an oral glucose test and a euglycaemic hyperinsulinaemic glucose clamp to establish baseline characteristics, and then again following the four months of supplementation. Plasma vitamin E concentrations increased significantly in all subjects taking the vitamin E supplement, compared to controls. In diabetic subjects, vitamin E supplementation reduced glucose area under the curve, and increase glucose disappearance, total glucose disposal and non-oxidative glucose metabolism compared to the type 2 diabetic control group. In the healthy subjects, vitamin E supplementation reduced the area under the curve (AUC) for glucose, and increased whole body glucose disposal and non-oxidative metabolism.
These results suggest that vitamin E in high doses is able to improve the action of insulin in both type 2 diabetic subjects and normal healthy subjects. The authors reported no side effects of the supplementation in any subject suggesting that levels of vitamin E of this magnitude are safe for long-term consumption. Interestingly the increase in vitamin E seen in the subjects correlated with the increase in the GSH to GSSG ratio, membrane microviscosity, total body glucose disposal, non-oxidative glucose disposal and the percentage change in oxygen production. All of these parameters were correlated with each other. The authors hypothesised that the vitamin E may be restoring levels of glutathione that then improves the structural integrity of membranes with respect their use of glucose. Vitamin C is also known to increase the GSH to GSSG ratio and so may have a similar effect as to that of vitamin E. The beneficial glycaemic effects of phytonutrients such as anthocyanins may also be explained through this same mechanism.
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