Absence of growth hormone-induced avian muscle growth in vivo

Abstract

Growth hormone (GH) clearly has the potential to dramatically enhance skeletal muscle accretion in red meat animals such as swine. It is generally accepted that this anabolic effect is mediated by insulin-like growth factor-I (IGF-I), a potent stimulator of proliferation and differentiation of satellite cells that are important for myofiber hypertrophy and for regeneration in postnatal muscle tissue. All available evidence suggests that the capacity for IGF-I-mediated actions of GH on avian myogenic cells is intact, and recent evidence is accumulating that GH may even have direct effects on avian skeletal muscle satellite cell proliferation and differentiation. However, with little exception, exogenous GH does not improve skeletal muscle mass, carcass protein, or any measure of muscle anabolism in domestic poultry. A primary lesion would appear to be the inability of GH to induce significant increases in circulating IGF-I concentrations in sexually immature, growing poultry. This is the case despite clear evidence of GH binding to hepatic receptors, GH-induced tyrosine phosphorylation of Janus kinase 2 (JAK2), and GH-induced expression of hepatic IGF-I mRNA and protein. Factors that should be explored with respect to this apparent discrepancy are discussed, including the regulation of IGF-I release, uptake, and interaction with cell-associated IGF binding proteins or receptors. In addition to its growth-promoting effects via IGF-I, GH has direct metabolic effects that are expressed as changes in circulating regulatory hormone and metabolite concentrations. The possibility that such changes may influence IGF-I release and action is also proposed.