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IGF-1 deficiency impairs endothelial NO bioavailability through elevation of NO breakdown due to increased generation of reactive oxygen species (ROS) and downregulation of endothelial nitric oxide synthase (eNOS) [168, 169]

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This is in accordance with preclinical studies demonstrating the ventral tegmental area and NAc as key areas mediating the effects of GLP-1 receptor agonists on alcohol intake 10,18