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Exp Mol Med

Demonstrating peripheral effects by suppressing T-cell-mediated inflammation via GLP-1 receptor activation in intestinal lymphocytes, and central effects by mediating Toll-like receptor (TLR)-induced anti-inflammatory responses through GLP-1 receptor signaling in the brain [39]

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The effects of glucagon in the liver also suggest paradoxical situations, such as those related to protein synthesis in fasting periods through transient protein kinase mechanistic target of rapamycin 1/2 (mTORC1/2) activation thanks to the GTPase activity of RAP-1 aided by exchange protein activated by cAMP (EPAC)