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Similarly, testosterone-enhanced mitochondrial enzymes implied increased energetic and oxidative demand, which PWE mitigated, consistent with its antioxidant activity

These findings indicate that the upstream signaling pathways necessary for NET formation are preserved in XKR8-deficient BMNs

This selectivity represents a fundamental difference from not only full-length growth hormone but also growth hormone secretagogues and analogs like tesamorelin, which increase endogenous growth hormone and subsequently elevate IGF-1

Overall, these findings highlight that LC and LAC may be a promising treatment for recovering REDOX status and mitochondrial dysfunction in the CNS in obesity