Fig 2: Treatment effects on muscle hypertrophy and atrophy in SAMP8 mice upon different time points. (A–C) Expression of IGF-1, MyoD, MyoG, Myf5 and Myf6 mRNA in different treatment groups at month 2, 3 and 4. (D) MuRF1 and MAFbx mRNA expression levels in the VIB group were significantly lower than in the Con group at month 4. (E,F) Western blots of protein expressions of mTOR, PI3K-p85, Akt, pAkt, p70-S6K, EIF4EBP1, MyoD and GAPDH at month 2, 3 and 4. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001, n = 3.

Fig 3: Carbidopa-mediated suppression of IDO1 in tumor cells inhibits mTORC1 signaling pathway.(A and B) Western blotting showing protein expression of S6K and 4EBP1 (total and phospho-form) in carbidopa-treated BxPC-3 and HPAF-II cell lines, which were also treated with MG132 to rule out protein degradation. β-actin was used as an endogenous control.

Fig 4: The inhibition of activation and differentiation of T cells was mediated by mTOR signaling. Freshly separated spleen cells were stimulated with 1.5 mg/ml ConA with or without treating 2.5μM DON, and cells were collected and proteins were extracted 24h after ConA stimulation. Western blotting was applied to analyze the levels of phosphorylated mTOR (A) and phosphorylated P70S6K (B). Data were expressed as means ± SEM. ***P <0.001.

Fig 5: Signal transduction proteins involved in the protein machinery in the TA after overnight fasting (Fasted) or supplementation with whey, P4 or casein. (A) 4EBP1 ratio between phosphorylated and total 4EBP1, (B) phosphorylated protein of 4EBP1, (C) total protein of 4EBP1, (D) p70S6K ratio between phosphorylated and total p70S6K, (E) phosphorylated protein of p70S6K, (F) total protein of p70S6K, (G) mTOR ratio between phosphorylated and total mTOR, (H) phosphorylated protein of mTOR, and (I) total protein of mTOR. Values are means ± SEM of both experiments and are expressed as a relative ratio to the fasted control group. * p < 0.05 compared to the fasted control group.