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“Appetite suppression via ketone bodies” is not a single molecular target or receptor but rather describes a physiological phenomenon observed during ketosis—whether induced by a ketogenic diet or exogenous administration of ketones. The main circulating ketone body, β-hydroxybutyrate (βHB), is associated with reduced hunger and blunted increases in ghrelin secretion that typically accompany weight loss. This effect appears to be mediated through multiple mechanisms including direct modulation of gut-derived hormones like ghrelin, GLP‑1, and CCK; possible central nervous system actions; and newly discovered metabolic shunt pathways involving BHB-amino acid conjugates that suppress feeding behaviors. While this phenomenon has therapeutic implications for obesity management and possibly other metabolic conditions, it does not correspond to a discrete druggable protein or receptor but rather an integrated metabolic state involving several molecular mediators[1][4][5][6].\n\nNote: This entry is considered incorrect as a canonical therapeutic target because it refers to a physiological process rather than an individual molecule or receptor amenable to direct pharmacological targeting.
Suppression of ghrelin secretion (“hunger hormone”)\n- Increase in satiety peptides such as GLP‑1 and cholecystokinin (CCK)\n- Modulation of neuroendocrine pathways in the hypothalamus by β-hydroxybutyrate and other ketone bodies[1][4][6]\n- Direct action of specific metabolites such as BHB-amino acids on feeding behavior[5]
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