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The phrase "modulation of gut hormones affecting appetite/satiety/glucose metabolism" does not refer to a single molecular target or defined protein but rather describes a physiological process involving several peptide hormones secreted by the gastrointestinal tract. The most prominent among these are peptide tyrosine–tyrosine (PYY), glucagon-like peptide 1 (GLP‑1), cholecystokinin (CCK), and ghrelin. These hormones regulate appetite and energy balance by acting on both peripheral tissues and central nervous system pathways that control hunger and fullness. For example, PYY, GLP‑1, and CCK have anorexigenic effects—suppressing appetite—while ghrelin is orexigenic—increasing hunger[1][3]. Drugs targeting this system typically act as agonists at specific receptors such as the GLP‑1 receptor to promote satiety or improve glucose metabolism in conditions like obesity or type 2 diabetes[3]. However, "modulation of gut hormones" is not itself a discrete therapeutic target but an umbrella term for interventions aimed at altering levels or activity of these various peptides[1][3]. Because this entry refers to a broad mechanism rather than a single molecule/receptor/protein with an established canonical name or abbreviation—and because it encompasses multiple targets—it should be flagged as incorrect for structured database purposes. For structured data extraction or drug discovery work, each individual gut hormone/receptor should be listed separately with its own canonical name—for example "Glucagon-like peptide 1 receptor" for drugs like liraglutide/semaglutide/exenatide[3].
Agonism of gut hormone receptors to enhance satiety and reduce food intake (e.g., GLP‑1 receptor agonists) *Note*: Mechanisms depend on the specific gut hormone and its corresponding drug.
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