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"Satiety hormones" is not a single molecule or therapeutic target but rather an umbrella term referring to several peptide and protein hormones that regulate feelings of fullness after eating. Key examples include glucagon-like peptide 1 (GLP‑1), peptide YY (PYY), cholecystokinin (CCK), leptin, amylin, ghrelin (which stimulates hunger rather than satiety), and somatostatin. These molecules act through distinct receptors—often G protein-coupled receptors—primarily within the gut-brain axis to modulate appetite control, energy balance, glucose metabolism, lipid metabolism, and body weight regulation. Drugs that mimic or antagonize these hormonal signals are important in treating obesity and related metabolic disorders. However, "satiety hormones" itself does not refer to any one molecular entity suitable for direct drug targeting—it represents a functional category comprising multiple targets with diverse mechanisms of action.
Mechanisms depend on the specific hormone but include: Agonism/antagonism at peptide hormone receptors to modulate appetite signaling pathways - For example, GLP‑1 receptor agonists enhance satiety signaling; somatostatin analogues inhibit growth hormone release and slow gastrointestinal transit; PYY analogues activate Y2 receptors to reduce food intake.
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