THE ROLE OF ROSIGLITAZONE IN MODULATING HDL CHOLESTEROL IN TYPE 2 DIABETES

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The third update of the National Cholesterol Education Program reclassifies diabetes mellitus as a cardiovascular risk equivalent and increased the lower limit for HDL cholesterol levels in the risk assessment for CAD. Of the different pharmacological agents used in the management of type 2 DM, the PPAR agonists have been shown to effectively lower blood glucose and improve lipids. Rosiglitazone significantly increases HDL, but the mechanism is unclear. The metabolism of HDL is complex and involves ABC transporters, scavenger receptors (SR-B1), cholesterol ester transfer protein (CETP) and hepatic lipase. The major goal of the study is to understand the mechanism by which rosiglitizone increases HDL. This study examines the lipoprotein subfractions, hepatic lipase activity, and expression and function of ABCA1 and SR-B1 in macrophages isolated from subjects with type 2 diabetes mellitus treated with rosiglitazone for 26 weeks.