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Immediately after cessation of semaglutide treatment, food intake significantly increased to levels above those observed in vehicle-treated mice ( Figure 2A-B )

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At the molecular level, ginsenosides mediate these effects primarily by activating the AMPK/SIRT1/PGC1- axis to promote mitochondrial biogenesis, engaging the PI3K/Akt/mTOR pathway to support muscle protein anabolism, and suppressing NF-B-driven inflammatory signaling to limit exercise-induced muscle damage

Using compromised reagents for any experiment undermines the principles of good scientific practice