title: Acute hyperglycaemia and oxidative stress generation.
abstract: Oxidative stress is an acknowledged pathogenic mechanism in diabetic complications. Several studies have demonstrated that acute hyperglycaemia can impair the physiological homeostasis of important systems in living organisms and that it may exert these effects via production of free radicals and associated oxidative stress. Acute increases in plasma glucose concentration may increase free radical production by the following mechanisms: labile glycation; auto-oxidation of glucose; and intracellular activation of the polyol pathway, which produces an imbalance in the NADH/NAD+ ratio and favours the production of free radicals. The hypothesis that free radicals may mediate the effects of acute hyperglycaemia is supported by evidence that antioxidants can counteract some of the effects induced by acute hyperglycaemia, for example, vasoconstriction, activation of coagulation, and the increase in plasma intracellular adhesion molecule-1 concentrations. Direct evidence of an association between oxidative stress and hyperglycaemia has come from studies of induced hyperglycaemia or standardized meal intake. In both diabetic and non-diabetic subjects, hyperglycaemia or meal intake causes a reduction in plasma Total Radical-trapping Antioxidant Parameter (TRAP). This is associated with consumption of protein thiol groups, vitamin C, and uric acid. This may confirm the hypothesis that acute hyperglycaemia provokes oxidative stress, which destroys the natural antioxidant defences found in the plasma.
authors.affiliation: University of Udine, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Ceriello
mesh_terms: D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000150:complications* / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*
chemical_list: D005609:Free Radicals; D018799:Intercellular Adhesion Molecule-1