Improved metabolic control that enhances insulin sensitivity and preserves beta-cell function may decrease platelet reactivity and improve the efficacy of antiplatelet agents in diabetic patients.
eople with diabetes, particularly those with type 2 diabetes, exhibit increased platelet reactivity. Hyperglycemia contributes to greater platelet reactivity through direct effects and by promoting glycation of platelet proteins. Hypertriglyceridemia increases platelet reactivity. Both insulin resistance and insulin deficiency increase platelet reactivity. Insulin antagonizes activation of platelets. Thus, relative or absolute deficiency of insulin would be expected to increase platelet reactivity. Diabetes is associated with oxidative stress and inflammation. Resultant endothelial dysfunction promotes activation of platelets by decreasing production of nitric oxide (NO) that attenuates platelet reactivity. Oxidative stress accentuates this effect by attenuating activity of NO and promoting platelet activation. Inflammation and platelet activation are reciprocally related. Inflammation promotes platelet activation that, in turn, promotes inflammation. Accordingly, improved metabolic control achieved with regimens that improve insulin sensitivity and preserve pancreatic -cell function is likely to decrease platelet reactivity and enhance effects of antiplatelet agents.
David J. Schneider (Tue,) studied this question.