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However, at pharmacological concentrations achieved with therapeutic GLP-1 receptor agonists (100 pM10 nM), -arrestin-2 becomes essential for sustained signaling, specifically mediating extracellular signal-regulated kinase (ERK) activation and CREB phosphorylation that promotes pancreatic -cell survival and insulin synthesis

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76 Thus, since PI3K/Akt is activated by both cAMP-dependent and cAMP-independent pathways, there is likely context-dependent variability in GLP-1R signaling, influenced by cell type, receptor architecture, and duration of stimulation