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Glucagon activates hepatic glycogenolysis and gluconeogenesis acutely, but its chronic effects are distinctly catabolic: Hepatic fat oxidation : Glucagon promotes beta-oxidation of fatty acids in the liver, directly reducing hepatic steatosis Thermogenesis : Glucagon increases resting energy expenditure through activation of brown adipose tissue and futile metabolic cycling Amino acid catabolism : Glucagon promotes hepatic amino acid uptake and ureagenesis Lipolysis : Glucagon stimulates adipose tissue lipolysis, mobilizing stored fat for oxidation The critical pharmacological challenge with survodutide is balancing glucagon's hyperglycemic potential against GLP-1's glucose-lowering effects