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At the same time, key metabolites in the longissimus dorsi, such as N,N,N-trimethyllysine, L-carnitine, and betaine, along with the key gene MPO , promoted intramuscular fat deposition by inhibiting fat oxidation and promoting fat synthesis (Figs

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Mechanistic analysis revealed that AR directly promoted the transcription of miR-221, which in turn suppressed IGF-1 expression, leading to the inactivation of the MAPK pathway in DPCs and the PI3K/AKT pathway in DSCs