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The satiety signaling pathway is not a single molecule or receptor but rather a complex physiological network that regulates the sensation of fullness and the cessation of eating after food intake. This system integrates signals from the gastrointestinal tract—such as stomach distension and nutrient detection—with hormonal messengers including glucagon-like peptide 1 (GLP‑1), cholecystokinin (CCK), peptide YY, leptin, and insulin. These hormones act primarily on the hypothalamus in the brain to modulate appetite and energy balance[4][7][8]. The gut-brain axis plays a central role in this process by relaying information about meal size and composition via neural pathways and circulating peptides. Pharmacological interventions targeting components of this pathway—such as GLP‑1 receptor agonists—are used clinically for obesity management by enhancing satiety signals to reduce caloric intake[3][5]. Disruption or dysregulation within this network can contribute to overeating and metabolic diseases like obesity. Because "satiety signaling pathway" refers to an integrated biological process rather than a discrete molecular target or druggable entity, it is not considered a therapeutic target itself but encompasses several targets within its framework. Note: This entry is marked as incorrect for use as a canonical drug target because it describes an entire physiological process rather than an individual molecule/receptor suitable for direct pharmacologic targeting. For structured data purposes, specific molecules such as "Glucagon-like peptide 1 receptor" or "Cholecystokinin A receptor" should be used instead when referencing actionable targets within this system[7][2].
Modulation of gut hormone release to enhance satiety or suppress appetite
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