Altered glucose metabolism and hypoxic response in alloxan-induced diabetic atherosclerosis in rabbits.

摘要: Diabetes mellitus accelerates atherosclerosis that causes most cardiovascular events. Several metabolic pathways are considered to contribute the development of atherosclerosis, but comprehensive alterations atherosclerotic arterial cells remain unknown. The present study investigated changes and their relationship vascular histopathological in arteries rabbits with alloxan-induced diabetes. Diabetic was induced rabbit ilio-femoral by injecting alloxan (100 mg/kg), injuring using a balloon, feeding 0.5% cholesterol diet. We histologically assessed lesion development, cellular content, pimonidazole positive-hypoxic area, nuclear localization hypoxia-inducible factor-1α, apoptosis. evaluated metabolism performing metabolomic analyses capillary electrophoresis-time flight mass spectrometry. glucose uptake its hypoxia 18F-fluorodeoxyglucose pimonidazole. Plaque burden, macrophage hypoxic areas were more prevalent diabetic, than non-diabetic atherosclerosis. Metabolomic highlighted 12 metabolites significantly altered between diabetic A half them associated glycolysis metabolites, levels decreased as lesions increased according content or non-diabetic, not rabbits. Despite profound areas, factor-1α number apoptotic lesions. Altered an impaired response under conditions insulin-dependent diabetes might be involved