Recent data suggest that changes in HDL and LDL could also influence beta cell function and mass, implying a role for lipoprotein particles in the pathogenesis of type 2 diabetes mellitus (T2DM). It was reported that ABCA1 deletion provokes cholesterol accumulation in the beta cell membrane and subsequently inhibits insulin secretion. It was also suggested that HDLs can inhibit beta cell apoptosis. HDLs are reported to enhance cellular glucose uptake in cultures of primary human skeletal muscle cells isolated from patients with T2DM. Thus, basic experimental studies display that HDLs have improve glucose homeostasis by both preserving beta cell function and by enhancing skeletal muscle glucose uptake. Recent clinical data also suggest that lipid and lipoprotein profiles can be independently associated with development of T2DM both in cross-sectional and longitudinal studies. I would present the data on the relation between lipoproteins and glucose metabolism.