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Satiety signaling pathways in the gut–brain axis comprise a complex set of neural and hormonal interactions that enable the gut to inform the brain about nutrient intake, meal size, and composition, ultimately leading to the sensation of fullness and termination of eating. These pathways involve enteroendocrine cells in the gut that release peptides such as GLP-1, cholecystokinin, and peptide YY in response to food intake. These signals reach the brain (especially the hypothalamus and brainstem) directly through the bloodstream or indirectly by activating vagal afferents, integrating into the central nervous system’s appetite control centers. Disruption or dysregulation of these pathways is implicated in obesity, metabolic syndrome, and eating disorders, and they are the focus of current pharmacological therapies aimed at appetite suppression and metabolic disease treatment.
Mimic gut hormones that trigger satiety; Inhibit neuronal signaling that promotes hunger; Modulate vagal afferent signaling to the brain; Block or stimulate neurotransmitter release from the gut or within the CNS.
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