No edit summary
|
|
||
(32 intermediate revisions by 23 users not shown) | |||
Line 1: | Line 1: | ||
'''Satiety''' ([[Help:IPA/English|/səˈtaɪ.ə.ti/]] [[Help:Pronunciation respelling key|''sə-TYE-ə-tee'']]) is a state or condition of fullness gratified beyond the point of satisfaction, the opposite of [[Hunger (physiology)|hunger]]. Following satiation (meal termination), satiety is a feeling of fullness lasting until the next meal.<ref>{{cite journal | vauthors = Hetherington MM | title = Sensory-specific satiety and its importance in meal termination | journal = Neuroscience and Biobehavioral Reviews | volume = 20 | issue = 1 | pages = 113–117 | date = 1996-01-01 | pmid = 8622817 | doi = 10.1016/0149-7634(95)00048-J | s2cid = 24305458 }}</ref> 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 a state or condition of fullness gratified beyond the point of satisfaction. It means you're not hungry any more. The satiety center in animals are located in [[ventromedial nucleus]] of hypothalamus. |
|||
The satiety center in animals is located in [[ventromedial nucleus]] of the [[hypothalamus]].<ref>{{cite journal | vauthors = Obradovic M, Sudar-Milovanovic E, Soskic S, Essack M, Arya S, Stewart AJ, Gojobori T, Isenovic ER | display-authors = 6 | title = Leptin and Obesity: Role and Clinical Implication | journal = Frontiers in Endocrinology | volume = 12 | pages = 585887 | date = 2021 | pmid = 34084149 | pmc = 8167040 | doi = 10.3389/fendo.2021.585887 | doi-access = free }}</ref> |
|||
⚫ | |||
== Mechanism == |
|||
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 nerve fiber|afferent]] vagus nerve fibers to the hypothalamus, increasing satiety.<ref name=":0">{{cite journal | vauthors = Tack J, Verbeure W, Mori H, Schol J, Van den Houte K, Huang IH, Balsiger L, Broeders B, Colomier E, Scarpellini E, Carbone F | display-authors = 6 | title = The gastrointestinal tract in hunger and satiety signalling | journal = United European Gastroenterology Journal | volume = 9 | issue = 6 | pages = 727–734 | date = July 2021 | pmid = 34153172 | pmc = 8280794 | doi = 10.1002/ueg2.12097 }}</ref> |
|||
== Signalling factors == |
|||
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.<ref name=":0" /> This effect is used to increase weight loss and treat obesity through GLP-1 agonists.<ref>{{cite journal | vauthors = Shi Q, Wang Y, Hao Q, Vandvik PO, Guyatt G, Li J, Chen Z, Xu S, Shen Y, Ge L, Sun F, Li L, Yu J, Nong K, Zou X, Zhu S, Wang C, Zhang S, Qiao Z, Jian Z, Li Y, Zhang X, Chen K, Qu F, Wu Y, He Y, Tian H, Li S | display-authors = 6 | title = Pharmacotherapy for adults with overweight and obesity: a systematic review and network meta-analysis of randomised controlled trials | language = English | journal = Lancet | volume = 399 | issue = 10321 | pages = 259–269 | date = January 2022 | pmid = 34895470 | doi = 10.1016/S0140-6736(21)01640-8 | s2cid = 244970524 }}</ref> [[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|date=August 2022}}{{short description|State of being filled or satisfied|noreplace}} |
|||
== See also == |
|||
*[[Satiety value]] |
|||
* [[Prader–Willi syndrome]] |
|||
== References == |
|||
{{reflist}} |
|||
[[Category:Digestive system]] |
[[Category:Digestive system]] |
||
[[Category:Neuropsychology]] |
|||
[[Category:Nutritional physiology]] |
|||
⚫ |
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.
The satiety center in animals is located in ventromedial nucleus of the hypothalamus.[2]
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]
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.[citation needed]
This medical article is a stub. You can help Wikipedia by expanding it. |