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Additive mechanisms: central activation of GLP-1R / GIPR hypothalamic satiety circuits, slowed gastric emptying, amplified glucose-dependent insulin secretion, direct adipocyte lipolysis via GCGR, brown thermogenesis via UCP1, and increased hepatic lipid oxidation

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Our data also document changes in other specific hypothalamic signaling pathways that may be related to the metabolic effects of the multi-agonist, as is the case of calcium/calmodulin-dependent protein kinase 2 (CAMK2)