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Isoproterenol inhibits resistin gene expression through a G S ‐protein‐coupled pathway in 3T3‐L1 adipocytes
Author(s) -
Fasshauer Mathias,
Klein Johannes,
Neumann Susanne,
Eszlinger Markus,
Paschke Ralf
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02588-1
Subject(s) - resistin , medicine , endocrinology , 3t3 l1 , forskolin , adenylyl cyclase , gs alpha subunit , chemistry , protein kinase a , gene expression , adipocyte , biology , insulin resistance , adipose tissue , insulin , kinase , gene , stimulation , adiponectin , biochemistry
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.