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¹ State Key Laboratory of Medical Genomics, Shanghai Institute of Endocrine and Metabolic Diseases, Center of Molecular Medicine, Ruijin Hospital, Shanghai Jiaotong University Medical School, 197, Ruijin Road II, Shanghai 200025, China
² Department of Endocrinology, The Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, China
³ Department of Endocrinology, Renji Hospital, 1630, Dongfang Road, Pudong, Shanghai 210127, China

(Request for offprints should be addressed to H Song; Email: huaidong_s1966{at}163.com; M Chen; Email: mingdaochensh{at}yahoo.com)

^* (G Yuan, X Chen and Q Ma contributed equally to this work)

C-reactive protein (CRP) is considered as one of the most sensitive markers of inflammation. The aim of the present study is to investigate the effects of CRP on the production of adiponectin in 3T3-L1 adipocytes. Northern and western blot analysis revealed that CRP treatment inhibited adiponectin mRNA expression and secretion in a dose- and time-dependent manner. Co-incubation of adipocytes with rosiglitazone and CRP decreased induction of adiponectin gene expression by rosiglitazone. However, luciferase reporter assays did not show that CRP affected the activity of ~2.1 kb adiponectin gene promoter, which was increased by rosiglitazone alone. Pharmacological inhibition of phosphatidylinositol (PI)-3 kinase by LY294002 partially reversed inhibition of adiponectin gene expression by CRP. These results collectively suggest that CRP suppresses adiponectin gene expression partially through the PI-3 kinase pathway, and that decreased production of adiponectin might represent a mechanism by which CRP regulates insulin sensitivity.

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