Cardiovascular diseases are the leading cause of death during diabetes, and qualitative changes in lipoproteins play a role in the pathogenesis of atherosclerosis. Hyperglycaemia induces glycation of lipoproteins, particularly low-density lipoproteins (LDL), preventing the recognition of apoprotein B by the specific receptor and favouring the accumulation of LDL in macrophages and their oxidation. Other effects contribute to increased LDL oxidation in diabetes: higher production (and decreased degradation) of free radicals, the association of hypertriglyceridemia with the presence of small, dense, more easily oxidizable LDL, and high-density lipoprotein anomalies which reduce LDL antioxidant capacities. Glycation- oxidation interactions are complex. Although glycated LDL are more easily oxidizable, antioxidants could also reduce protein glycation independently of glycaemic balance. The role of glyco-oxidative changes in the pathogenesis of atherosclerosis during diabetes is difficult to determine, partly because of methodological problems related to the presence of circulating antioxidants which allow only minimal (and not easily demonstrable) LDL oxidation. The development of measurements sensitive to lipoprotein oxidation should facilitate the determination of LDL oxidative status. The main means of preventing and treating glyco-oxidative alterations are the normalisation of LDL-cholesterol concentrations and the improvement of glycaemic balance. Prospective studies are needed to determine the role of antioxidants in the prevention and/or treatment of atheromatous disease during diabetes.