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To better understand the biological basis underlying skeletal muscle growth efficiency in ducks, this study systematically examined the key developmental transition from late embryogenesis (E19, E24) to early post-hatch stages (P1, P10). Histological analyses revealed that post-hatch muscle growth was primarily characterized by progressive myofiber hypertrophy. Systemically, insulin-like growth factor 1 (IGF1) protein levels, but not IGF2, increased in both serum and liver following hatching. In contrast, targeted gene expression analysis demonstrated that IGF1 and IGF2 expression in liver and skeletal muscle was dynamically and independently regulated in a stage-specific manner, supporting a predominant role for local IGF signaling. This tissue-autonomous program was further supported by the coordinated temporal expression of key myogenic regulators (MYOD1, MYF5, PAX7) and differentiation markers (MYH1B, MYF6). Notably, the metabolic nuclear receptor farnesoid X receptor (FXR) showed tissue-specific expression, being markedly induced in the liver but suppressed in skeletal muscle after hatching. Moreover, FXR expression was more closely associated with local IGF and myogenic regulatory networks than with circulating IGF levels. Collectively, these findings demonstrate that post-hatch skeletal muscle development in ducks is governed by precise tissue-specific regulatory programs and suggest FXR as a potential molecular link between metabolic signaling and local muscle growth pathways.
CHEN et al. (Thu,) studied this question.