How does platelet stimulation by a variety of agonists lead to activation and platelet aggregation? We are interested in elucidating the signalling pathways that are involved in platelet activation, in particular those that may play a role in platelet hyperactivity in conditions such as obesity and diabetes. Platelets are able to respond to a wide range of agonists and when activated at the site of injury they rapidly aggregate to form a platelet haemostatic plug. Increased or inappropriate platelet activation, however, will lead to thrombosis and vascular complications. Risk factors such as obesity and some genetic factors lead to a resistance to insulin, which is the major underlying cause of type II, adult-onset diabetes, the most common type of diabetes. Type II diabetes is associated with an increased risk of cardiovascular complications, which is the main cause of morbidity and mortality in these patients. There is substantial evidence for platelet hyperactivity in patients with diabetes, which is thought to play a contributory role in diabetic heart disease. Although, the pathogenesis of diabetic cardiovascular disease is not yet fully understood, it is likely to involve the clustering of certain risk factors, often called the insulin resistance syndrome, which is associated with type II diabetes. In our lab, we are interested in investigating the contribution of these risk factors to making platelets hyper responsive.