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Examining direct GLP-1R-mediated cardiomyocyte protection through PI3K-Akt and AMPK pro-survival pathway activation in cardiac ischaemia-reperfusion models, endothelial GLP-1R-mediated anti-inflammatory and anti-atherosclerotic biology, the relative contributions of direct cardiac GLP-1R signalling versus systemic metabolic improvements through weight and glucose reduction to cardiovascular outcome benefits, and the mechanistic basis of GLP-1R-mediated plaque stabilisation, endothelial function improvement, and cardiac remodelling attenuation

the confirmatory secondary endpoint was change in bodyweight, both after 40 weeks of treatment

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