Insulin, which physiologically reduces platelet responses to agonists both in vitro [77–79] and in vivo [77, 80, 81], mainly through a NO-dependent mechanism mediated by the increase of intraplatelet cyclic nucleotides 3′, 5′ -cyclic guanosine monophosphate (cGMP) and 3′, 5′ -cyclic adenosine monophosphate (cAMP) [78, 82], exhibits a deeply impaired antiaggregating effect in insulin resistant states, such as central obesity, type 2 diabetes mellitus with obesity and essential arterial hypertension [81, 83–85]. Here, INS is linked to diabetes mellitus.