Diabetes type 2: magnitudes of agonist-evoked platelet activity markers in vitro demonstrate a substantial individual dependence

In type 2 diabetes (T2DM), of the pathways and magnitudes of whole blood agonist-evoked responses, that is, platelet reactivity is not well understood. This study aimed to identify mechanisms regulating platelet reactivity in T2DM. The study included 35 individuals with T2DM. A flow cytometer analyzed whole blood agonist-evoked [α-thrombin (10 μmol/l) (α-thr), collagen (0.15 μg/ml) (coll), ADP (5 μmol/l)] surface phosphatidylserine (annexin V) expressions, fibrinogen receptor activities (PAC-1), and lysosomal exocytosis (LAMP-1) (all fluorescence intensities of normal-sized platelets). The correlation coefficient ( r ) compared induced activity markers for each agonist and agonist variations of platelet reactivity. Collagen-evoked and ADP-evoked annexin responses were inversely associated with PAC-1 (coll: r = -0.6, ADP: r = -0.7). Additionally, after provocation, annexin V and LAMP-1 were related contrariwise (all agonists: r = -0.5). Agonist-induced PAC-1 correlated with LAMP-1 expressions (α-thr: r = 0.5, coll: r = 0.6, ADP: r = 0.7). The study demonstrated that induced annexin V was closely associated (α-thr vs. coll: r = 0.9, α-thr vs. ADP: r = 0.7, coll vs. ADP: r = 0.9). PAC-1 (α-thr vs. coll: r = 0.8, α-thr vs. ADP: r = 1.0, coll vs. ADP: r = 0.8) and LAMP-1 (α-thr vs. coll: r = 0.7, α-thr vs. ADP: r = 0.8, coll vs. ADP: r = 0.5) displayed similar relationships. The magnitudes of agonist-evoked reactions in vitro are associated, and the agonist category proved less significant for regulating agonist-induced activity. Close inverse correlations between agonist-evoked annexin V and both PAC-1 and LAMP-1 suggest that procoagulant reactions after provocation directed platelet activity. Thus, reactivity is regulated by platelet characteristics connected to the T2DM individuals.