Diabetes mellitus is a problem of health worldwide being vascular complications the main causes of morbidity and mortality in this population. Diabetics have a fast atherothrombotic evolution which is worse than that observed for other clinical entities; however, hyperglycemia itself may not totally explain the ischemic complications observed in these patients. Most ischemic arterial events are precipitated by plaque rupture, platelet activation, and thrombosis. Several abnormalities in the blood coagulation system have been described associated to diabetes mellitus, all of them predisposing to thrombosis: endothelial cell dysfunction, platelet hyperreactivity, thrombin generation and hypofibrinolysis. Platelets play a key role in diabetic atherothrombosis due to platelet hypersensitivity to physiological agonists, low response to therapeutical antiplatelet agents, platelet hyperreactivity in sites of endothelial cell damage, hyperaggregability, resistance to the inhibitory effects of the insulin, and low endothelial production of prostacyclin and nitric oxide. All these phenomena have been associated to either a toxic microenvironment due to hyperglycemia or to intrinsic platelet abnormalities. Based on all these facts, it is proposed that platelets may be another target for the negative effects of insulin-resistance state. Because platelets are crucial in the atherosclerotic process and in the genesis of the vascular complications of diabetes mellitus, this review analyses the platelet abnormalities observed in this metabolic disease.