Horm Metab Res 2011; 43(7): 464-469
DOI: 10.1055/s-0031-1277226
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Aldosterone Perturbs Adiponectin and PAI-1 Expression and Secretion in 3T3-L1 Adipocytes

P. Li1 , 2 , [*] , X.-N. Zhang2 , [*] , C.-M. Pan2 , F. Sun2 , D.-L. Zhu1 , H.-D. Song2 , M.-D. Chen2
  • 1Department of Endocrinology, Drum Tower Hospital Affiliated to Nanjing University Medical School, Nanjing, P. R. China
  • 2Ruijin Hospital, Shanghai Institute of Endocrinology, State Key Laboratory of Medical Genomics, Molecular Medicine Center, Shanghai Jiao Tong University (SJTU) School of Medicine, P. R. China
Further Information

Publication History

received 20.02.2011

accepted 19.04.2011

Publication Date:
10 June 2011 (online)

Abstract

Aldosterone is considered as a new cardiovascular risk factor that plays an important role in metabolic syndrome; however, the underlying mechanism of these effects is not clear. Hypoadiponectinemia and elevated circulating concentration of plasminogen activator inhibitor-1 (PAI-1) are causally associated with obesity-related insulin resistance and cardiovascular disease. The aim of the present study is to investigate the effect of aldosterone on the production of adiponectin and PAI-1 in 3T3-L1 adipocytes. Northern and Western blot analyses revealed that aldosterone treatment inhibited adiponectin mRNA expression and secretion and simultaneously enhanced PAI-1 mRNA expression and secretion in a time- and dose-dependent manner. Rosiglitazone did not prevent aldosterone's effect on adiponectin or PAI-1 expression. In contrast, tumor necrosis factor (TNF)-α produced dramatic synergistic effects on adiponectin and PAI-1 expression when added together with aldosterone. Furthermore, the effects of aldosterone on adiponectin and PAI-1 expression appear to be mediated through glucocorticoid receptor (GR) but not mineralocorticoid receptor (MR). These results suggest that the effects of aldosterone on adiponectin and PAI-1 production are one of the underlying mechanisms linking it to insulin resistance, metabolic syndrome and cardiovascular disease.

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1 These authors contributed equally to this work.

Correspondence

H.-D. Song
M.-D. Chen

Ruijin Hospital

Shanghai Institute of

Endocrinology

State Key Laboratory of Medical

Genomics

Molecular Medicine Center

Shanghai Jiao Tong University

(SJTU) School of Medicine

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P. R. China

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