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The critical roles of these residues are highlighted by mutagenesis studies, where D198 2.68b A, K202 2.72b A, L388 7.43b A and L388 7.43b I abolished GLP-1(9-36)-induced cAMP accumulation, but still allowed GLP-1(7-36) signaling ( Fig

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95% CI, 1.01-3.07) over a 2-year follow-up period