High fructose diets have been shown to induce insulin resistance within a few weeks when fed to rats. Studies involving rats were initially criticised because the amount of fructose used was deemed too high to be relevant to human nutrition. However, subsequent analysis has shown that fructose consumption by humans is within the range of intakes used in rat studies. Further, human studies involving the feeding of lower doses of fructose have resulted in insulin resistance within a short time period. Fructose is able to cause insulin resistance when consumed in its refined crystalline form, including when present as a disaccharide in the sucrose molecule (table sugar). Fructose is thought to switch the metabolism of the liver towards de novo lipogenesis, or the formation of fatty acids from carbohydrate sources. The resultant fatty acids are exported to tissues, where they accumulate in tissues and cause insulin resistance by an unknown mechanism, possibly involving oxidative stress.
If oxidative stress is involved in the aetiology of insulin resistance, it might be expected that antioxidant nutrients be beneficial at preventing the insulin resistant state. Researcher have assessed a number of antioxidants in this role and found beneficial effects at improving insulin sensitivity. Many such studies have involved animal models. For example, in one study1, researchers fed three groups of rats different diets. One group served as the control and these rats received normal rat chow. Another group of rats were fed a high carbohydrate diet that comprised of 60 % of the carbohydrates as fructose. Such a diet has been used previously to induce insulin resistance in rats in a short period of time, perhaps as little as two weeks. A third group of rats were fed the same high carbohydrate high fructose diet, but they were also fed 3.4 grams of vitamin E per kg of diet. The rats were fed these diets for 6 weeks and following this time they were assessed for insulin resistance and levels of oxidative stress.
The results showed that the high carbohydrate high fructose diet significantly deteriorated the insulin sensitivity of the rats. In addition the high carbohydrate high fructose fed rats also experienced a significant increase in levels of oxidative stress, as measured by an increase in lipid peroxidation rates, increased oxidised glutathione blood levels and reduced superoxide dismutase activity. The vitamin E fed rats also experiences both insulin resistance and increase oxidative stress compared to the controls, but the levels were not as high as in those rats consuming the high carbohydrate high fructose diet without the vitamin E. Therefore vitamin E appears to ameliorate some of the detrimental effects of a high fructose diet, suggesting that some of the contributory changes that result in insulin resistance may be related to oxidative stress. This data is supported by many other studies that show improvements in insulin sensitivity with consumption of foods that are high in antioxidants.
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