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– Mechanism:
Satiety is signaled through the vagus nerve and circulating hormones.
– Stomach stretches during a meal to accommodate increased volume.
– Gastric accommodation activates stretch receptors in the upper stomach.
– Receptors signal to the hypothalamus through afferent vagus nerve fibers.
– This process increases satiety.

– Signalling factors:
– Duodenal cells release substances affecting digestion and satiety.
– Glucagon-like peptide-1 (GLP-1) inhibits stomach relaxation.
– GLP-1 increases stretch of the stomach and slows gut motility.
– Cholecystokinin (CCK) slows gut motility and increases satiety.
– CCK activates release of pancreatic enzymes and bile.

– See also:
Satiety value.
– Prader–Willi syndrome.

– References:
– Hetherington MM (1996-01-01). Sensory-specific satiety in meal termination.
– Obradovic M et al. (2021). Leptin and Obesity: Role and Clinical Implication.
– Tack J et al. (July 2021). The gastrointestinal tract in hunger and satiety signaling.
– Shi Q et al. (January 2022). Pharmacotherapy for adults with overweight and obesity.
– Various medical articles on satiety and related topics.

– Categories:
– Medicine stubs.
– Digestive system.
– Neuropsychology.
– Nutritional physiology.
– Articles with short description and unsourced statements.

Satiety (Wikipedia)

Satiety (/səˈtaɪ.ə.ti/ sə-TYE-ə-tee) is a state or condition of fullness gratified beyond the point of satisfaction, the opposite of hunger. Following satiation (meal termination), satiety is a feeling of fullness lasting until the next meal. When food is present in the GI tract after a meal, satiety signals overrule hunger signals, but satiety slowly fades as hunger increases.

The satiety center in animals is located in ventromedial nucleus of the hypothalamus.

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