Nuclear respiratory factor and peroxisome proliferator activated receptor gamma co-activator-1-dependent oxidative metabolic pathways may play a central, and potentially primary, role in the pathogenesis of type 2 diabetes.
Other diabetes-specific factors, such as increased levels of plasminogen activator 1 and fibrinogen, chronic inflammation, genetic susceptibility, and accelerated glycosylation end-products-mediated vascular damage, are thought to play a role in the development of CVD among patients with type 2 diabetes.
Obesity is associated with prothrombotic changes which have been well-characterised and include increased levels of plasminogen activator-1, von Willebrand factor, fibrinogen and evidence of increased coagulation and platelet activation; however, these changes do not seem to account for all the increased risk.