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This version published online on August 19, 2004
Endocrinology, doi:10.1210/en.2004-0503
A more recent version of this article appeared on December 1, 2004
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Submitted on April 19, 2004
Accepted on August 12, 2004

Induction of adiponectin in skeletal muscle by inflammatory cytokines: in vivo and in vitro studies

Aurélie M. Delaigle, Jean-Christophe Jonas, Isabelle B. Bauche, Olivier Cornu, and Sonia M. Brichard*

Endocrinology and Metabolism Unit, Orthopaedic Research Laboratory, University of Louvain, Faculty of Medicine, 1200 Brussels, Belgium

* To whom correspondence should be addressed. E-mail: brichard{at}endo.ucl.ac.be.

Adiponectin (ApN) is an adipocytokine that plays a fundamental role in energy homeostasis and in counteracting inflammation. We examined whether ApN could be induced in a non-adipose tissue, the skeletal muscle, in vivo and in cultured myotubes in response to lipopolysaccharides (LPS) or pro-inflammatory cytokines. We next explored the underlying mechanisms. In vivo, injection of LPS to mice caused, after 24 h, a ~10-fold rise in ApN mRNA abundance and a concomitant 70% increase in ApN levels in tibialis anterior muscle. This ApN induction was reproduced in C2C12 myotubes cultured for 48 h with a pro-inflammatory cytokine combination, IFN{gamma} + TNF{alpha}. This effect occurred in a time- and dose-dependent manner. Several pieces of evidence suggest that NO mediates this up-regulation by cytokines in myotubes or muscle. First, ApN was induced in vitro exclusively in the experimental conditions that stimulated NO production. Second, iNOS mRNA induction or NO production clearly preceded ApN mRNA induction. Third, preventing NO production by inhibitors of the NO synthases, L-NAME or L-NNMA, suppressed the inductive effect of the cytokines in vitro and in vivo. Finally, ApN mRNA induction by cytokines was reproduced in cultured human myotubes. In conclusion, our data provide evidence that adiponectin is upregulated in vivo and in vitro in human and rodent myotubes in response to inflammatory stimuli. The underlying mechanisms seem to involve a NO-dependent pathway. This overexpression may be viewed as a local anti-inflammatory protection and a way to deliver extra energy supplies during inflammation.
Key words: Adiponectin • cytokines and muscle




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