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"Dietary fiber" is not a single molecule or receptor but a broad class of plant-derived carbohydrates that are resistant to digestion in the human small intestine. Dietary fibers increase satiety through several mechanisms including mechanical effects such as increased chewing and gastric distention; delayed gastric emptying; modulation of gut hormones like cholecystokinin (CCK), glucagon-like peptide 1 (GLP‑1), and peptide YY (PYY); production of short-chain fatty acids via fermentation by the gut microbiota; and reduced energy density in foods. These actions collectively contribute to reduced hunger sensations, prolonged fullness after meals, decreased subsequent food intake, improved metabolic parameters such as glucose and insulin levels, suppression of appetite-stimulating hormones like ghrelin, and potential weight loss or prevention of weight gain. However, "dietary fiber increasing satiety" is not itself a molecular therapeutic target but rather describes a physiological effect mediated by multiple pathways involving various receptors and signaling molecules.[1][2][3][4][6] **Note:** There is something incorrect about this target entry—“dietary fiber increasing satiety” does not refer to a specific molecule or receptor but rather describes an effect produced by dietary fibers acting through multiple biological mechanisms. Therefore: - **is_target:** false Dietary fibers are not considered classical drug targets like receptors or enzymes. - **is_incorrect:** true The entry refers to an effect/phenotype rather than a discrete molecular entity suitable for structured drug targeting. If you need information on specific molecular targets involved in dietary-fiber-induced satiety—such as GLP‑1 receptor or PYY receptor—please specify which one for more precise data.
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