Ethanol is thought to have particular metabolic effects that induce the oxidation of fatty acids. This may include stimulation of MEOS (microsomal enzyme oxidising system) in the liver. While chronic intakes of ethanol are detrimental to the liver because they increase the production of fatty acids and increase tissue accumulation of lipids leading to alcoholic fatty liver, more moderate intake may actually decrease fatty acid accumulation through increased oxidation. This may explain the inverse association between alcohol consumption and bodyweight. As fatty acids are thought to induce insulin resistance, ethanol may have protective effects against the development of insulin resistance and its associated diseases. As red wine is a source of ethanol, some of the benefits of red while at preventing the symptoms of the metabolic syndrome may therefore come from the ethanol component (here). However, evidence also suggests that resveratrol, a polyphenol derived from grapes and present in wine, may also be beneficial.
Observations suggests that resveratrol (3,5,4’-trihydroxystilbene), may be an antidiabetic agent in animals. In particular, resveratrol may have blood glucose lowering effects. Rats with artificially induced diabetes were fed resveratrol at various concentrations and compared to control rats1. In the diabetic rats, blood glucose was reduced by 4.2 % with administration of resveratrol. when compared to rats receiving no resveratrol. In addition, the plasma triglyceride concentrations of the rats were reduced by between 2.2 and 3.2 % compared to controls receiving no resveratrol. The blood glucose lowering effects of resveratrol were accompanied by decreases in the insulin concentrations in the rats and a delay to the point of insulin resistance. This suggests that resveratrol may have insulin sensitising effects in rats. Glucose uptake was increased in skeletal muscle, liver and adipocyte tissue, and this uptake was additional to that produced by insulin, suggesting that resveratrol works through alternate mechanism to insulin.
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