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Articles in PresS, published online ahead of print July 2, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00054.2002
Submitted on February 7, 2002
Accepted on June 20, 2002
* To whom correspondence should be addressed. E-mail: laura.fernandez{at}diab.ucl.ac.be.
The role of tumor necrosis factor (TNF)- in muscle catabolism is well established but little is known about the mechanisms of its catabolic action. One possibility could be that TNF- impairs the production of local growth factors like Insulin-like Growth Factor (IGF)-I. The aim of this study was to investigate whether TNF- can directly inhibit IGF-I gene and protein expression in muscle. First, we investigated whether the acute inflammation induced by endotoxin injection changes IGF-I and TNF- mRNA in rat tibialis anterior muscle. Endotoxin rapidly increased TNF- mRNA (7-fold at 1 h; P<0.001) and later decreased IGF-I mRNA (-73% at 12 h; P<0.001). Furthermore, in a model of C2C12 myotubes TNF- strongly inhibited IGF-I mRNA and protein (-73% and -47% after 72 h; P<0.001 and P<0.01 respectively). Other proinflammatory cytokines failed to inhibit IGF-I mRNA. The effect of TNF- on IGF-I mRNA was not mediated by nitric oxide and the activation of NFkB was insufficient to inhibit IGF-I expression. Taken together our data suggest that TNF- induced in muscle after LPS injection can locally inhibit IGF-I expression. The inhibition of muscle IGF-I production could contribute to the catabolic effect of TNF-.
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