Atherosclerosis is the major cause of death in the diabetic population. Hyperglycaemia per se is an independent risk factor for the development of cardiovascular disease, in spite of the coexistence of other known risk factors, such as hyperlipidaemia and hypertension [1,2]. Elevated concentrations of low density lipoproteins (LDL) are also a major risk factor in the general population [3,4]. However, LDL levels are usually normal in both insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes (NIDDM) [2,5].It has been postulated that the increased cardiovascular risk for diabetic patients could be related, among other factors, to LDL qualitative modifications such as oxidation and glycation. These modifications impair LDL cellular catabolism, leading to loss of affinity for LDL receptors in fibroblasts, increased accumulation of cholesteryl esters in macrophages, and immunological responses [6,7]. In Diabetologia (1996) Summary We evaluated the effect of improving glycaemic control with intensive insulin therapy on LDL susceptibility to oxidation, electronegative LDL proportion, and LDL subfraction phenotype in a group of 25 patients with short-duration insulin-dependent diabetes mellitus (IDDM); 25 matched healthy control subjects were also studied. LDL susceptibility to oxidation was measured by continuous monitoring of conjugated diene formation. Electronegative LDL was isolated by anion exchange chromatography, and quantified as percentage of total LDL. Six LDL subfractions were isolated by density gradient ultracentrifugation and phenotype A or B classified as the quotient (LDL1-LDL3)/(LDL4-LDL6). Compared to the control group, IDDM subjects with poor glycaemic control showed higher electronegative LDL (19.03 ± 10.09 vs 9.59 ± 2.98 %, p < 0.001), similar LDL subfraction phenotype and lower susceptibility to oxidation (lag phase 45.6 ± 8.8 vs 41.2 ± 4.7 min, p < 0.05). After three months of intensive insulin therapy, HbA 1 c decreased from 10.88 ± 2.43 to 5.69 ± 1.54 % (p < 0.001), and electronegative LDL to 13.84 ± 5.15 % (p < 0.05). No changes in LDL susceptibility to oxidation or LDL subfraction phenotype were observed. Electronegative LDL appeared significantly correlated to HbA 1 c and fructosamine (p < 0.01 and p < 0.001) only in poorly controlled IDDM patients. These findings suggest that high electronegative LDL in IDDM subjects is related to the degree of glycaemic control, and could therefore be due to LDL glycation rather than to LDL oxidation or changes in LDL subfraction phenotype.