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It establishes cellular antioxidant defense by transcriptionally activating antioxidant genes (e.g., SOD2, CAT, GCL) and reductive molecules (e.g., GSH, Trx), while downregulating pro-oxidant molecule synthesis, thereby directly scavenging or neutralizing excess ROS [134]

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A second mechanism of PKA-independent incretin potentiation of glucose-stimulated insulin secretion (GSIS) involves cAMP-regulated guanine nucleotide exchange factor (cAMP-GEF) EPAC2