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Unlike the above models, in which activation of sAC was studied after injury, we demonstrate that GLP-1(2836) acts as a preconditioning agent by activating sAC through increased production of ATP, leading to downstream cAMP/PKA activation

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They blunt activation of nuclear factor kappa B (NFB), reducing transcription of inflammatory mediators, and promote anti-inflammatory signaling and metabolic equilibrium via AMP-activated kinase (AMPK) activation

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