Table 2.

Compilation of the most important results of GLP-1 and GLP-1R agonists from animal studies mentioned in the text

	GLP-1	References	GLP-1R agonist	References
	Elicits cAMP in mouse cardiomyocytes	[38]	mRNA Expression is localized in cardiac atria and and its activation promotes secretion of atrial natriuretic peptide and increases BP.	[11,31,64]
	Inhibits palmitate- and ceramide-induced phosphatidylserine exposure and DNA fragmentation	[44]	Acts via cAMP in endosome	[37]
	Increases myocardial glucose uptake in dogs	[46]	Decreases myocyte apoptosis by activation of cAMP/PKA/CREB pathway	[39]
	May preserve cardiomyocyte viability, increases metabolic efficiency and inhibits the structural and functional remodeling after myocardial infarction.	[49]	Induces cardiomyocyte growth and activation of glucose metabolism by a mechanism envolving AKT and ERK phosphorylations	[24,40,41]
Animals studies	Increases systolic and diatolic BP, as well as HR im male rats acutely.	[52]	Has cardioprotective functions related to inhibition of cardiomyocytes apoptosis due their ROS scanvenger actions, by increasing endogenous antioxidant defenses.	[42]
	Inhibts glucagon release by a mechanism PKA dependent and glucose independent	[16,17]	Cardioprotective functions are mediated by PI3K and partially dependent on ERK1/2	[43]
	Decreases contractility in primary culture of adult rat cardiomyocytes and in isolated rat hearts	[45,76]	Attenuates atherosclerotic lesions by reducing monocyte/macrophage accumulation in the arterial wall and inhibits the inflammatory response in macrophages.	[65]
			Reduces the inflammatory markers: MCP-1 and TNF-α in response to lipopolysaccharide in cultured peritoneal macrophages harvested from mice.	[66]
			Reduces monocyte adhesion to aortic endothelial cells and atheroscleroticlesion size in nondiabetic C57BL/6 and ApoE−/− mice.	[65]