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Figure 1 | BMC Surgery

Figure 1

From: Randomized control trial to evaluate the effects of acute testosterone administration in men on muscle mass, strength, and physical function following ACL reconstructive surgery: rationale, design, methods

Figure 1

Akt1 signaling and control of skeletal muscle hypertrophy and atrophy. Anabolic signals (e.g. testosterone) initiate phosphorylation (P) of Akt1, which activates protein synthesis via the mTOR pathway. At the same time, Akt1(P) inactivates FOXO3a by phosphorylation and facilitates translocation of FOXO3a out of the nucleus, resulting in inhibition of the atrophy-related genes (atrogens), and thereby decreasing protein degradation. On the other hand, catabolic stimuli (e.g. glucocorticoids) dephosphorylate and thereby inactivate the Akt1 protein. Inactivation of the Akt1 protein allows expression of FOXO3a in the nucleus and subsequent activation of the atrogens, resulting in protein degradation. (Figure adapted from G.A. Nader) [10].

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