It has been demonstrated that type 2 diabetes mellitus can induce compositional differences in LDL (increased apoCIII/apoB molar ratio) and increase the binding of LDL to arterial proteoglycans.24 At least in the hyperinsulinemic model studied here, it seems that non–lipid-associated differences in remnant lipoprotein composition do not play a large role in exacerbating particle binding with arterial proteoglycans ex vivo. This evidence concerns the gene APOB and type 2 diabetes mellitus.