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Anaya Malik | AMJ

But, if you arent quite sure what they actually are, heres a little refresher

2d, e) to test whether the hepatic TH signaling was responsible for the elevation of GLP-1 and insulin levels observed in above experiments

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While GLP-1 agonists primarily reduce appetite and slow gastric emptying (decreasing energy intake), glucagon agonism actively promotes calorie burning through multiple pathways: Hepatic lipid mobilization: Glucagon signals the liver to break down stored fat for energy Brown fat thermogenesis: Preclinical data suggests glucagon activation promotes heat generation in brown adipose tissue Increased fatty acid oxidation: The body shifts toward using fat stores as fuel, even at rest In essence, retatrutide attacks obesity from both sides: reducing what goes in (appetite suppression via GLP-1 and GIP) while increasing what goes out (energy expenditure via glucagon)