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Background/Aims   Myostatin belongs to the transforming growth factor‐β superfamily and negatively regulates skeletal muscle mass. Its deletion induces muscle overgrowth, while, on the contrary, its overexpression or systemic administration cause muscle atrophy. The present study was aimed at investigating whether muscle depletion as occurring in an experimental model of cancer cachexia, the rat bearing the Yoshida AH‐130 hepatoma, is associated with modulations of myostatin signalling and whether the cytokine tumour necrosis factor‐α may be relevant in this regard.

Materials and methods   Protein levels of myostatin, follistatin (myostatin endogenous inhibitor) and the activin receptor type IIB have been evaluated in the gastrocnemius of tumour‐bearing rats by Western blotting. Circulating myostatin and follistatin in tumour hosts were evaluated by immunoprecipitation, while the DNA‐binding activity …