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Glucagon naturally increases energy expenditure and promotes fat oxidation

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Semaglutide selectively activates the GLP-1 receptor, producing: Glucose-dependent insulin secretion : Reduces hypoglycemia risk compared to non-incretin agents Glucagon suppression : Reduces hepatic glucose output in the hyperglycemic state Gastric emptying delay : Contributes to postprandial glucose control and satiety Central appetite regulation : Acts on GLP-1 receptors in the hypothalamus and brainstem to reduce hunger and alter food preferences The simplicity of semaglutide's single-receptor mechanism is both a limitation (no energy expenditure enhancement from glucagon) and a strength (thoroughly understood pharmacology, predictable effects, extensive safety characterization)

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