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This cAMP-dependent effect is mediated via both PKA and Epac [48,90] and cAMP analogues that activate both PKA and Epac can substitute for GLP-1 by inducing CICR in the presence of Ca 2+ [87]
The short answer is no, not yet
It is possible that the anti-inflammatory CRP reductions observed in the STEP and SELECT trials require the full doses used in those studies
Pancreatic islets and cells also express GLP-1R, therefore GLP1 binding can also inhibits glucagon and stimulates somatostatin release (de Heer, Rasmussen, Coy & Holst, 2008
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