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

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。第三次更新的国家胆固醇教育计划将糖尿病重新分类为心血管风险当量，并提高了冠心病风险评估中高密度脂蛋白胆固醇水平的下限。在用于治疗2型糖尿病的不同药理学药物中，PPAR激动剂已被证明能有效降低血糖和改善血脂。罗格列酮显著增加HDL，但机制尚不清楚。HDL的代谢是复杂的，涉及ABC转运蛋白、清道夫受体（SR-B1）、胆固醇酯转移蛋白（CETP）和肝脂肪酶。该研究的主要目的是了解罗格列酮增加HDL的机制。本研究检测了接受罗格列酮治疗26周的2型糖尿病患者巨噬细胞中脂蛋白亚组分、肝脂肪酶活性以及ABCA1和SR-B1的表达和功能。

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.