Lipoprotein glycation in atherogenesis

There has been increasing interest in investigating the role of glycation as an atherogenic modification of lipoproteins; especially after the failure of antioxidant therapy to suppress the incidence of atherogenic cardiovascular diseases in high-risk individuals. Glycation of lipoproteins impairs their function. In the case of LDL, it also leads to rapid scavenger-receptor uptake by monocyte/macrophages. Glycation also diminishes the antiatherogenic properties of HDL. The concentration of circulating glycated LDL, even in nondiabetics, is higher than that of oxidatively modified LDL. Glycated small dense LDL is significantly higher in nondiabetic individuals as well as in Type 2 diabetic patients. Lowering the level of small dense LDL by using statins lowers glycated LDL in Type 2 diabetic patients. This may be one of the reasons for their effect in decreasing cardiovascular risk in these patients. Treatments that prevent glycation of lipoproteins may prevent atherosclerosis and other diabetic complications.