**8. Conclusion**

T1DM is associated with platelet hypersensitivity to stimulating agonists. Hyperglycemia, in a dose and duration-dependent manner, provides the substrates for energy generation that powers alpha granule translocation to the membrane surface. Enhanced expression of P-selectin and GPIIbIIIa contributes to increased platelet aggregation evident in T1DM. Platelet hyperactivity in T1DM represents a reversal of the attenuating effects of low dose or physiological insulin. This is augmented by the attendant hyperlipidemia. However, the paradoxical hyperactivity in the presence of hyperinsulinemia is due to counter-regulatory hormones and

potentiation by insulin-like growth factor. Overall, platelet activation in T1DM occurs through multiple signal transduction pathways not targeted by currently available antiplatelet agents. These pathways offer avenues for the development of novel antiplatelet remedies with improved therapeutic efficacy.
