Fructose fed rats develop insulin resistance in just a short period. In some cases high intakes of refined crystalline fructose, or refined crystalline sucrose, causes insulin resistance in rats in just a few weeks. The development of fructose induced insulin resistance in rats is a useful model for humans because along with the insulin resistance the rats develop nonalcoholic fatty liver, high triglyceride levels, excessive body fat, cardiovascular disease and diabetes. In other words feeding rats high fructose diets causes the same metabolic syndrome as seen when humans eat fructose. Antioxidant nutrients have been shown to protect rats from the metabolic syndrome when fed high fructose diets. Antioxidants are likely helpful because oxidative stress may be a causative factor in insulin resistance. That red wine is beneficial at inhibiting the metabolic changes associated with fructose diets is therefore no surprise because it is an excellent source of dietary antioxidants, particularly the stilbene resveratrol which belongs to the polyphenol group.
However, when a group of fructose fed rats were exposed to red wine components, it was not the polyphenolic antioxidants, which include resveratrol, that was the most effective insulin sensitising component of red wine1. Observations in fact showed that ethanol was the most beneficial component within the wine for preventing metabolic deterioration caused by the fructose induced insulin resistance. The polyphenols were observed to protect from left ventricular hypertrophy and as expected provided a reduction in oxidative stress in the tissues of the animals. The polyphenol component also contributed to a reduction in plasma glucose levels. However, it was the ethanol within the wine that was largely responsible for the sensitisation of the insulin receptor and the lowering of plasma insulin levels. As evidence suggests that ethanol may be able to stimulate the oxidation of fatty acids, this may explain the insulin sensitising effects of ethanol, at least in rats.
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