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Gastrointestinal hormone pathways regulating satiety comprise a complex network of endocrine signals released by the gut in response to nutrient ingestion to signal fullness to the central nervous system. Key components include hormones such as glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), and cholecystokinin (CCK), which primarily act through specific G protein-coupled receptors located on vagal afferents and in brain regions like the hypothalamus and area postrema. These pathways play a critical role in energy homeostasis by inhibiting food intake and slowing gastric motility. Dysregulation of these systems is a hallmark of obesity and metabolic disease, making them primary targets for pharmacological intervention. Modern therapeutics, particularly GLP-1 and GIP receptor agonists, leverage these pathways to achieve significant weight loss and glycemic control in patients with obesity and type 2 diabetes.
Activation of G protein-coupled receptors (e.g., GLP-1R, GIPR) to stimulate satiety centers in the hypothalamus and hindbrain, delay gastric emptying, and modulate insulin/glucagon secretion.
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