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These data are consistent with previous reports demonstrating that -arrestin 1/2 are indispensable for the potentiating action of GLP-1 on glucose-stimulated insulin secretion in cultured pancreatic cells 6,7

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In comparison to the marked differences between N-terminally substituted exendin-4 agonist responses, differential effects on binding kinetics, -arrestin recruitment, internalization, and recycling were relatively modest within these licensed compounds, albeit statistically significant in some cases (Fig

Similarly, CJC-1295 selectively activates GH