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Health News Archive 140 - Diabetes
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Quercetin Reverses Oxidative Damage in Diabetic Rats

Quercetin blocks free radical damage in diabetic rats, indicating it may prevent the development of tissue injury seen in diabetics, researchers reported in the October 2005 Journal of Nutrition.

Both experimental and clinical studies have produced evidence that suggests oxidative stress caused by free radicals is involved in the development and progression of diabetic tissue damage. Consequently, the researchers of the current study investigated quercetin’s effects on markers of oxidative stress in diabetic rats.

Researchers divided the animals into four groups. 1) One group served as the untreated, healthy controls. 2) Another group of healthy, non-diabetic animals received quercetin administered intraperitoneally (by way of the abdomen). 3) A third group of diabetic animals remained untreated while a 4) fourth group of diabetic rats received an injection of quercetin administered intraperitoneally.

Eight weeks later, the researchers measured levels of markers of oxidative stress in the animals. They also measured levels of antioxidant enzymes.

Plasma glucose was significantly increased in the diabetic animals and quercetin administration had no effect on this. Markers of oxidative stress were also increased in the untreated diabetic animals; however, in the diabetic animals given quercetin, these markers of oxidative stress were markedly reduced or abolished. Quercetin also blocked the production of harmful mediators that triggered the production of oxidative stress in the untreated diabetic animals.

The researchers concluded that quercetin “may block the production of noxious mediators involved in the development of early diabetes tissue injury and in the evolution of late complications.”

Reference:

Dias AS, Porawski M, Alonso M, Marroni N, Collado PS, Gonzalez-Gallego J. Quercetin Decreases Oxidative Stress, NF-{kappa}B Activation, and iNOS Overexpression in Liver of Streptozotocin-Induced Diabetic Rats. J Nutr. 2005 Oct;135(10):2299-304.