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reported that GLP-1-induced suppression of glucagon release is dependent of protein kinase A (PKA) and independent of glucose or paracrine effects mediated by insulin or by somatostatin acting on somatostatin receptor subtype-2 [16],[17]

(October 1993)

At the start of the study, the median baseline body mass index among study participants was 38.5

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4,6 A key issue in the physiology of type 2 diabetes (T2DM) is the reduced incretin effect, which mainly results from decreased activity of the primary incretin hormones, GLP-1 (glucagon-like peptide 1) and GIP (glucose-dependent insulinotropic peptide)

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