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Laboratory studies suggest the peptide can shift gene-expression patterns toward a profile associated with younger tissue and may support the activity of cells involved in repair

GH facilitates growth via IGF-dependent pathways (hepatic secretion of IGF-1, and proliferation and maturation of IGF-sensitive, epiphyseal chondrocytes) and other direct, non-IGF-dependent mechanisms [53,54,55] In SAM, despite raised concentrations of GH, circulating IGF-1 levels remain low, possibly indicating a resistance to GH-mediated production of IGF-1 [44]