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.[1] When food is present in the GI tract after a meal, satiety signals overrule hunger signals, but satiety slowly fades as hunger increases.
Satiety is signaled through the vagus nerve as well as circulating hormones. During intake of a meal, the stomach must stretch to accommodate this increased volume. This gastric accommodation activates stretch receptors in the proximal (upper) portion of the stomach. These receptors then signal through afferent vagus nerve fibers to the hypothalamus, increasing satiety.[3]
Signalling factorsedit
In addition, as the food moves into the duodenum, duodenal cells release multiple substances that affect digestion and satiety. Glucagon-like peptide-1 (GLP-1) is an incretin released by the duodenum that inhibits relaxation of the stomach. This inhibition causes increased stretch of the stomach, increasing activation of proximal gastric stretch receptors. It also slows overall gut motility, increasing the duration of satiety.[3] This effect is used to increase weight loss and treat obesity through GLP-1 agonists.[4]Cholecystokinin (CCK) is gut peptide produced by the duodenum in response to fat and proteins. CCK has the effect of slowing gut motility and increasing satiety as well as activating release of pancreatic digestive enzymes and bile from the gallbladder.
^Hetherington MM (1996-01-01). "Sensory-specific satiety and its importance in meal termination". Neuroscience and Biobehavioral Reviews. 20 (1): 113–117. doi:10.1016/0149-7634(95)00048-J. PMID 8622817. S2CID 24305458.
^Obradovic M, Sudar-Milovanovic E, Soskic S, Essack M, Arya S, Stewart AJ, et al. (2021). "Leptin and Obesity: Role and Clinical Implication". Frontiers in Endocrinology. 12: 585887. doi:10.3389/fendo.2021.585887. PMC8167040. PMID 34084149.
^ abTack J, Verbeure W, Mori H, Schol J, Van den Houte K, Huang IH, et al. (July 2021). "The gastrointestinal tract in hunger and satiety signalling". United European Gastroenterology Journal. 9 (6): 727–734. doi:10.1002/ueg2.12097. PMC8280794. PMID 34153172.
^Shi Q, Wang Y, Hao Q, Vandvik PO, Guyatt G, Li J, et al. (January 2022). "Pharmacotherapy for adults with overweight and obesity: a systematic review and network meta-analysis of randomised controlled trials". Lancet. 399 (10321): 259–269. doi:10.1016/S0140-6736(21)01640-8. PMID 34895470. S2CID 244970524.
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satiety, səˈtaɪ, state, condition, fullness, gratified, beyond, point, satisfaction, opposite, hunger, following, satiation, meal, termination, satiety, feeling, fullness, lasting, until, next, meal, when, food, present, tract, after, meal, satiety, signals, o. Satiety seˈtaɪ e ti se TYE e 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 1 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 2 Contents 1 Mechanism 2 Signalling factors 3 See also 4 ReferencesMechanism editSatiety is signaled through the vagus nerve as well as circulating hormones During intake of a meal the stomach must stretch to accommodate this increased volume This gastric accommodation activates stretch receptors in the proximal upper portion of the stomach These receptors then signal through afferent vagus nerve fibers to the hypothalamus increasing satiety 3 Signalling factors editIn addition as the food moves into the duodenum duodenal cells release multiple substances that affect digestion and satiety Glucagon like peptide 1 GLP 1 is an incretin released by the duodenum that inhibits relaxation of the stomach This inhibition causes increased stretch of the stomach increasing activation of proximal gastric stretch receptors It also slows overall gut motility increasing the duration of satiety 3 This effect is used to increase weight loss and treat obesity through GLP 1 agonists 4 Cholecystokinin CCK is gut peptide produced by the duodenum in response to fat and proteins CCK has the effect of slowing gut motility and increasing satiety as well as activating release of pancreatic digestive enzymes and bile from the gallbladder citation needed See also editSatiety value Prader Willi syndromeReferences edit Hetherington MM 1996 01 01 Sensory specific satiety and its importance in meal termination Neuroscience and Biobehavioral Reviews 20 1 113 117 doi 10 1016 0149 7634 95 00048 J PMID 8622817 S2CID 24305458 Obradovic M Sudar Milovanovic E Soskic S Essack M Arya S Stewart AJ et al 2021 Leptin and Obesity Role and Clinical Implication Frontiers in Endocrinology 12 585887 doi 10 3389 fendo 2021 585887 PMC 8167040 PMID 34084149 a b Tack J Verbeure W Mori H Schol J Van den Houte K Huang IH et al July 2021 The gastrointestinal tract in hunger and satiety signalling United European Gastroenterology Journal 9 6 727 734 doi 10 1002 ueg2 12097 PMC 8280794 PMID 34153172 Shi Q Wang Y Hao Q Vandvik PO Guyatt G Li J et al January 2022 Pharmacotherapy for adults with overweight and obesity a systematic review and network meta analysis of randomised controlled trials Lancet 399 10321 259 269 doi 10 1016 S0140 6736 21 01640 8 PMID 34895470 S2CID 244970524 nbsp This medical article is a stub You can help Wikipedia by expanding it vte Retrieved from https en wikipedia org w index php title Satiety amp oldid 1205892134, wikipedia, wiki, book, books, library,
