60周年校庆系列讲座－－5月24日太田嗣人副教授:趋化因子系统在肥胖引起胰岛素抵抗过程中的功能研究

　　主讲人：太田嗣人副教授
　　地点：朝晖校区生环楼二楼大会议室
　　时间：2013年5月24日（周五）15:30
　　主办单位：生环学院
　　联系电话：88320387
    
　　主讲人简介：
　　Dr. Tsuguhito Ota (太田博士) ，2003年获得日本Kanazawa University（金泽大学）药学院博士学位，2008年在美国哥伦比亚大学完成博士后研究，随后回国任教于日本金泽大学前沿科学部。太田博士目前主要从事糖尿病相关研究，尤其在酒精与肝脏脂质代谢、胰岛素抵抗方面做了大量深入的研究工作。其研究成果已经在世界顶级SCI杂志，如NEW ENGL J MED（IF=53.484）、DIABETES（IF=8.889）、J CLIN INVEST（IF=14.152）等期刊上发表。现任美国糖尿病协会、欧洲糖尿病研究会以及日本糖尿病协会会员等。
    
　　讲座摘要：
　　C-C motif chemokine receptor (CCR)2 and its ligand, monocyte chemoattractant protein (MCP)-1, are pivotal for adipose tissue macrophage (ATM) recruitment and the development of insulin resistance. However, other chemokine systems also may play a role in these processes. In this study, we investigated the role of CCR5 in obesity-induced adipose tissue inflammation and insulin resistance. We analyzed expression levels of CCR5 and its ligands in white adipose tissue (WAT) of genetically (ob/ob) and highfat (HF) diet–induced obese (DIO) mice. Furthermore, we examined the metabolic phenotype of Ccr5-/- mice. CCR5 and its ligands were markedly upregulated in WAT of DIO and ob/ob mice. Fluorescence-activated cell sorter analysis also revealed that DIO mice had a robust increase in CCR5+ cells within ATMs compared with chow-fed mice. Furthermore, Ccr5-/- mice were protected from insulin resistance, glucose intolerance, and hepatic steatosis induced by HF feeding. The effects of loss of CCR5 were related toboth reduction of total ATM content and an M2-dominant shift in ATM polarization. It is noteworthy that transplantation of Ccr5-/- bone marrow was sufficient to protect against impaired glucose tolerance. CCR5 plays a critical role in ATM recruitment and polarization and subsequent development of insulin resistance.