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Satiety induction via delayed gastric emptying refers to the use of pharmacological or physiological mechanisms to slow the rate at which food leaves the stomach and enters the small intestine. This process increases feelings of fullness by prolonging stomach distension and enhancing signals from gut hormones such as cholecystokinin (CCK), glucagon-like peptide 1 (GLP‑1), and peptide YY (PYY) that communicate with the brain through neural pathways like the vagus nerve. These mechanisms are targeted therapeutically in obesity management—most notably by GLP‑1 receptor agonists—to reduce appetite and caloric intake. However, excessive delay can lead to symptoms such as nausea, vomiting, early satiety, bloating, nutritional deficiencies, and may contribute to conditions like gastroparesis.
Delay of gastric emptying to prolong stomach distension and enhance satiety signaling via gut-brain axis\nActivation of gut peptide hormone pathways that inhibit gastric motility and promote fullness (e.g., GLP‑1, CCK)
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