The detection of early atherosclerosis, accelerated by the presence of diabetes mellitus, is of major importance for improving the prediction and the prevention of subsequent clinical events. Three markers of atherosclerosis can be detected non invasively: arterial wall thickening, coronary calcification and arterial wall stiffening. Intima-media thickness can be measured by B-mode ultrasonography in common carotid and femoral arteries. Increased intima-media thickness has been found to be associated with both insulin-dependent and non insulin-dependent diabetes. Such thickening might be partly of atherogenic nature but may also be due to a non-atherogenic process such as medial hypertrophy possibly related to insulin effects. Coronary calcification, an anatomic marker of coronary atheroma, is detected radiographically by fluoroscopy or ultrafast computed tomography. Cross-sectional studies of asymptomatic high-risk populations have found independent associations between diabetes and the presence and amount of coronary calcium deposit. The mechanisms by which diabetes promotes coronary calcium deposit are unknown, but mineralization proteins, such as osteopontin and its genetic expression, might be implicated in the calcinosis process. Arterial wall stiffening, a marker of sclerosis, detected by pulse wave velocity measurement or by determination of arterial wall motion using an echotracking device, has been found to be associated with diabetes in several case-control and transverse studies. The mechanisms of such association may involve the effect of glycoregulation of bioelastomers in the arterial wall. The detection of early atherosclerosis in diabetic patients may be clinically relevant by helping to improve the prediction of vascular risk, the justification to treat, and the evaluation of the efficacy of antidiabetic treatment on the vessels.