Treatment with TNF-α and IFN-γ alters the activation of SER/THR protein kinases and the metabolic response to IGF-I in mouse c2c12 myogenic cells

Abstract

i) TNF-alpha and IFN-gamma, but not IL-1beta, if present in the extracellular environment during C2C12 myoblast differentiation, prevent the stimulatory action of IGF-I on protein synthesis. ii) TNF-alpha- and IFN-gamma-induced IGF-I resistance of protein synthesis could be associated with the decreased phosphorylation of PKB and p70(S6k). iii) The activation of glucose uptake in C2C12 myogenic cells treated with IFN-gamma is PKB independent. iv) The similar effects of TNF-alpha and IFN-gamma on the signalling and action of IGF-I on protein synthesis in myogenic cells could suggest the involvement of both of these cytokines in protein loss in skeletal muscle.