Abstract 9493: Plasma Levels Of Soluble CD36 In Type 2 Diabetes - A Link Between Platelet Activation, Inflammation And Oxidative Stress
INTRODUCTION Inflammation, oxidative stress and platelet activation are involved in the pathogenesis of type 2 diabetes (T2DM) and its complications. Soluble CD36 (sCD36) has been proposed to early identify diabetic subjects at risk of developing accelerated atherothrombosis.
HYPOTHESIS We aimed at characterizing the platelet contribution to sCD36 in T2DM, to correlate its formation with the extent of in vivo lipid peroxidation and to investigate the effects of low-dose aspirin on these processes.
METHODS A cross-sectional comparison of sCD36, soluble CD40L (sCD40L) as a marker of platelet-mediated inflammation, urinary 11-dehydro-TxB2 and 8-iso-PGF2α, in vivo markers of platelet activation and lipid peroxidation, respectively,was performed between 200 T2DM patients (94 of them on low-dose aspirin) and 47 healthy controls.
RESULTS sCD36 (median [IQR]: 0.72 [0.31-1.47] vs 0.26 [0.2-0.37], p=0.003) and urinary 11-dehydro-TxB2 levels (666 [293-1336] vs 279 [160-396], p≤0.0001) were significantly higher in T2DM patients not on aspirin (n=106) than in healthy subjects. These variables were significantly lower in aspirin-treated diabetics than in untreated patients (p<0.0001). Among patients not on aspirin, those with long-standing diabetes had significantly higher sCD36 levels in comparison to patients with diabetes duration <1 year (1.01 [0.62-1.86] vs 0.44 [0.22-1.21], p=0.001). Consistently, in the same group of patients, a significant linear correlation was found between sCD36 and diabetes duration (rho=0.347; p=0.0001), fasting blood glucose (rho=0.378; p=0.002) and HbA1c (rho=0.255; p=0.026). sCD36 linearly correlated with urinary 11-dehydro-TxB2, 8-iso-PGF2α and sCD40L in diabetics not on aspirin. On multiple regression analysis, 11-dehydro-TxB2 (β=0.360; SEM=0.0001, p=0.001), 8-iso-PGF2α (β=0.469; SEM=0.0001, p<0.0001) and diabetes duration (β=0.244; SEM=0.207, p=0.017) independently predicted sCD36 levels.
CONCLUSIONS sCD36 may be a link among hyperglycemia, inflammation, lipid peroxidation and platelet activation. Because it can only incompletely be down-regulated by low-dose aspirin, additional antiplatelet strategies in T2DM should be investigated to interrupt CD36-dependent platelet activation.
- © 2011 by American Heart Association, Inc.