Platelets and Diabetes

It is increasingly recognized that platelets are the culprit cells implicated in the propensity
to atherothrombosis in the setting of both type 1 and type 2 diabetes mellitus, making the
study of platelet pathophysiology and platelet activation/inhibition some of the most
intriguing fields of research related to diabetes vascular complications. Indeed, a platelet
hyperreactive phenotype with biochemical evidence of persistent in vivo platelet activa-
tion, with enhanced thromboxane (TX) biosynthesis, has been described in diabetic patients
in different stages along the natural history of the impairment of glucose metabolism, even
in the preclinical phases.
This chapter highlights several issues within this field: (1) the variable contribution of
sustained and acute hyperglycemia, glycemic instability, and insulin resistance to the
observed changes in the platelet pathophysiology; (2) the role of oxidative stress and
inflammation and namely of platelet-derived inflammatory molecules and microparticles,
as secondary mediators of diabetes-induced platelet activation; and (3) the complex
intertwining between the described pathophysiology and the anticipated epidemiological
burden in terms of high risk of vascular events and lower protection from antithrombotic
prophylaxis, with particular reference to aspirin.
Availability of high-throughput techniques is rapidly changing the way we address the
problem, with a deeper insight on transcriptomics and posttranscriptional regulation of
platelets as a consequence of the above-described metabolic abnormalities.