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Satiety signaling pathways refer collectively to the complex network of hormonal, neural, and central nervous system mechanisms that regulate feelings of fullness after eating. These integrated systems involve gut-derived peptide hormones such as cholecystokinin (CCK), glucagon-like peptide 1 (GLP‑1), peptide YY (PYY), amylin, insulin from pancreatic β-cells, and leptin from adipose tissue. These signals act on peripheral nerves—especially via vagal afferents—and central brain regions including the hypothalamus and brainstem nuclei. The primary function is to suppress hunger following food intake by integrating short-term meal-related cues with long-term energy status information. Disruption in these pathways can contribute to overeating and obesity. However, "satiety signaling pathways" is not a single molecular target but rather an umbrella term encompassing multiple interacting molecules and circuits involved in appetite control. "Satiety signaling pathways" is not a canonical name for any one molecule or druggable target; it describes an interconnected physiological process involving many distinct targets. For structured data purposes requiring specificity at the level of receptors or enzymes suitable for pharmacological intervention, this entry should be flagged as incorrect ("is_incorrect": true) because it does not correspond to a unique molecular entity.
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