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For example, it has been reported that activates the AMP-activated protein kinase (AMPK) (82), while the main regulatory factor is adaptability of the skeletal muscle oxidative metabolism, but interferes with mammalian target of rapamycin complex 1 (mTORC1) signaling, a major regulator of skeletal muscle hypertrophy (83, 84)

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Alternatively, the increased QUIN/KYN ratio in PTSD could also derive from a different distribution of KYN in body compartments, such as increased passage of this molecule through the BBB or its recruitment for binding to the aryl hydrocarbon receptor (Ahr) that promotes ROS modulation, all of which could potentially occur during the induction of cytokine release and inflammation present in these patients (142)

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