Isoproterenol inhibits resistin gene expression through a GS‐protein‐coupled pathway in 3T3‐L1 adipocytes

FEBS Letters

Fasshauer, Mathias²  Eszlinger, Markus²  Neumann, Susanne²  Paschke, Ralf²  Klein, Johannes¹ 

[1] Medical University of Lübeck, Department of Internal Medicine I, 23538 Lübeck, Germany;University of Leipzig, Department of Internal Medicine III, Ph.-Rosenthal-Str. 27, 04103 Leipzig, Germany

关键词: Resistin;    β-Adrenergic receptor;    Insulin resistance;    Obesity;    3T3-L1 adipocyte;    FFA;    free fatty acids;    Glut;    glucose transporter;    G-protein;    guanine nucleotide-binding protein;    RT-PCR;    reverse transcription-polymerase chain reaction;    T3;    triiodothyronine;    TZD;    thiazolidinedione;   

DOI  :  10.1016/S0014-5793(01)02588-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Resistin was recently identified as a hormone secreted by adipocytes which leads to insulin resistance in vivo and in vitro and might therefore be an important link between obesity and diabetes. To clarify the regulation of resistin gene expression, 3T3-L1 adipocytes were treated with various agents known to modulate insulin sensitivity, and resistin mRNA was measured by quantitative real-time reverse transcription-polymerase chain reaction. Interestingly, isoproterenol treatment reduced the level of resistin mRNA to 20% of non-treated control cells. This effect was dose-dependent with significant inhibition occurring at concentrations as low as 10 nM isoproterenol. Moreover, pretreatment of adipocytes with the β-adrenergic antagonist propranolol almost completely reversed the inhibitory effect of isoproterenol, whereas addition of the α-adrenergic antagonist phentolamine did not have any effect. Furthermore, the effect of isoproterenol could be mimicked by activation of G_S-proteins and adenylyl cyclase. Thus, both cholera toxin and forskolin decreased resistin mRNA expression in a dose-dependent fashion by up to 90% of control levels. Taken together, these results suggest that resistin gene expression is regulated by a protein kinase A-dependent pathway in 3T3-L1 adipocytes.

【 授权许可】

Unknown