Abstract : Type-2 diabetes and metabolic syndrome are associated with increased oxidative stress and cardiovascular risk. Platelet hyperactivation and dyslipoproteinemia are two major factors favoring atherothrombosis. We have shown that low-density lipoproteins (LDL) from type-2 diabetic patients activate platelets from healthy volunteers. The primary objective of our study was to establish the lipid and lipid peroxide profile of LDL isolated from plasma of volunteers with a metabolic syndrome (SM), of type-1 (DT-1) or type-2 (DT-2) diabetic patients compared to LDL from healthy volunteers (V). The second objective was to explore their role in platelet activation. Only LDL from MS and DT-2 groups have lipid abnormalities (increased triacylglycerols and decreased cholesteryl esters, decreased linoleic acid). LDL from SM, DT-1 and DT-2 groups show oxidative stress as assessed by increased lipid peroxide derivatives (hydroxylated fatty acids, malondialdehyde) and decreased plasmalogens. Compared to platelets incubated with LDL from the V group, platelets incubated with LDL from other groups are activated as shown by the enhancement of the arachidonic acid signalling cascade (p38 MAPK, cytosolic phospholipase A2, thromboxane B2). Thus, in a pre-diabetic state and in type-2 diabetes, LDL undergo lipid and oxidative modifications and activate platelets. Our results show that lipid peroxides in LDL could be the common denominator underlying platelet hyperactivation.