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Am J Physiol Endocrinol Metab (May 17, 2005). doi:10.1152/ajpendo.00090.2005
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Submitted on March 1, 2005
Accepted on May 11, 2005

Interleukin-6 is a negative regulator of visfatin gene expression in 3T3-L1 adipocytes

Susan Kralisch1, Johannes Klein2, Ulrike Lossner1, Matthias Bluher1, Ralf Paschke1, Michael Stumvoll1, and Mathias Fasshauer1*

1 Department of Internal Medicine III, University of Leipzig, Leipzig, Germany
2 Department of Internal Medicine I, University of Lubeck, Lubeck, Germany

* To whom correspondence should be addressed. E-mail: mathias.fasshauer{at}medizin.uni-leipzig.de.

Visfatin is a novel adipocytokine exerting insulin-mimetic effects in various insulin-sensitive tissues such as liver, muscle, and fat. In contrast, interleukin (IL)-6 is a proinflammatory adipose-secreted factor that induces insulin resistance and plasma concentrations of which correlate with the development of type 2 diabetes mellitus. In the current study, the impact of IL-6 on visfatin gene expression in 3T3-L1 adipocytes was determined by quantitative real-time reverse transcription-polymerase chain reaction. Interestingly, 30 ng/ml IL-6 time-dependently downregulated visfatin synthesis with a significant 40 % suppression seen after 4 h of treatment. Furthermore, addition of IL-6 for 16 h dose-dependently suppressed visfatin mRNA with significant effects first observed at concentrations as low as 3 ng/ml and a maximal 43 % reduction at 30 ng/ml effector. Moreover, inhibitor studies suggested that the negative effect of IL-6 on visfatin expression is, at least in part, mediated by p44/42 mitogen-activated protein kinase. In contrast, troglitazone did not reverse the negative effect of IL-6 on visfatin synthesis under these conditions. Taken together, our study suggests that IL-6 might influence glucose tolerance in part by regulation of the novel insulin-mimetic adipocytokine visfatin.




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