Hyperglycaemia: the bridge between non-enzymatic glycation and oxidative stress in the pathogenesis of diabetic complications.
It is generally accepted that high glucose levels for many years are a primary cause of most long-term complications in diabetic patients. Many studies suggest that the central features of diabetic complications are caused by the hyperglycaemia-accelerated formation of non-enzymatic glycated products. Non-enzymatic glycation, however, has been recently demonstrated to be linked to glucose auto-oxidative process. At the same time glycated proteins have been shown to be a source of free radicals. These findings raised the hypothesis of a link between oxidative stress and the development of diabetic complications. Some studies have recently demonstrated that antioxidants, such as vitamin C and E, may reduce in vitro and in vivo protein glycation. At the same time some antioxidants act as scavengers of the free radicals produced by non-enzymatic glycation in vitro. Such studies may lead to therapeutic approaches for limiting the damage from glycation and oxidation reactions and for complementing existing therapy for treatment of the complications of diabetes.
Ceriello
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University of Udine, Italy.
D001205:Ascorbic Acid / Q000502:physiology; D048909:Diabetes Complications; D005947:Glucose / Q000378:metabolism / Q000502:physiology; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000150:complications* / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D014810:Vitamin E / Q000502:physiology
D017127:Glycation End Products, Advanced; D014810:Vitamin E; D005947:Glucose; D001205:Ascorbic Acid