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"Satiety enhancement via increased protein intake" refers to the physiological effect whereby consuming higher amounts of dietary protein leads to greater feelings of fullness and reduced subsequent food intake. This effect is mediated through several mechanisms: > - **Slower gastric emptying** due to the longer digestion time required for proteins compared to carbohydrates or fats[1]. > - **Increased release of anorexigenic gut hormones** such as glucagon-like peptide 1 (GLP‑1), peptide YY (PYY), and cholecystokinin (CCK), which promote satiety signals in the brain while suppressing orexigenic hormone ghrelin that stimulates hunger[1][3][4]. > - **Elevated plasma amino acid concentrations**, which can act directly on the central nervous system to signal fullness ("aminostatic hypothesis")[2][3]. > - **Higher diet-induced thermogenesis**, meaning more energy expenditure after eating high-protein meals contributes indirectly to appetite regulation[2][3]. This concept does not refer to any specific receptor, enzyme, transporter, or other canonical therapeutic target but rather describes an integrated physiological response involving multiple pathways and molecules. Therefore it should not be considered a valid entry for structured drug-target databases focused on discrete molecular entities. If you are seeking information about specific receptors involved in mediating these effects—such as GLP‑1 receptor or PYY receptor—those would be appropriate canonical targets instead. In summary: "Satiety enhancement via increased protein intake" describes an important nutritional strategy for weight management but does not correspond to an individual molecule or therapeutic target suitable for structured pharmacological annotation[1][2][3].
Not applicable as this is not a discrete molecular target. Mechanisms involve modulation of gut hormones such as GLP‑1, PYY, CCK and suppression of ghrelin through increased amino acid and peptide levels from digested proteins[1][3][4][5].
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