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Unité de Diabétologie et Nutrition, Université catholique de Louvain, B-1200 Brussels, Belgium
The role of 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 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 NF-
B 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-.
skeletal muscle; lipopolysaccharide; C2C12 cells
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