The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Gastrointestinal Satiety Signals I. An overview of gastrointestinal signals that influence food intake
Abstract
An overview is presented of those signals generated by the gastrointestinal (GI) tract during meals that interact with the central nervous system to create a sensation of fullness and satiety. Although dozens of enzymes, hormones, and other factors are secreted by the GI tract in response to food in the lumen, only a handful are able to influence food intake directly. Most of these cause meals to terminate and hence are called satiety signals, with CCK being the most investigated. Only one GI signal, ghrelin, that increases meal size has been identified. The administration of exogenous CCK or other satiety signals causes smaller meals to be consumed, whereas blocking the action of endogenous CCK or other satiety signals causes larger meals to be consumed. Satiety signals are relayed to the hindbrain, either indirectly via nerves such as the vagus from the GI tract or else directly via the blood. Most factors that influence how much food is eaten during individual meals act by changing the sensitivity to satiety signals. This includes adiposity signals as well as habits and learning, the social situation, and stressors.
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Citations
Cites
A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans
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“This is true of CCK, bombesin-related peptides (GRP and NMB), GLP-1, apolipoprotein A-IV, and PYY-(3–36).”
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Cited by
Obesity Pathogenesis: An Endocrine Society Scientific Statement
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Signals that influence food intake and body weight
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Self-citationKoch, K. L., & Calles-Escandón, J. (2015) · Gastroenterology Clinics of North America · doi:10.1016/j.gtc.2014.11.005 · Cited by 92
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The Brain-Gut-Islet Connection
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Self-citation
Metadata
- Authors
- Woods, S. C.
- Venue
- American Journal of Physiology-Gastrointestinal and Liver Physiology
- Publisher
- American Physiological Society
- Published
- 2004-01
- Volume
- 286
- Issue
- 1
- Pages
- G7-G13
- ISSN
- 0193-1857 (ISSN-L)
- 1522-1547
- OpenAlex
- W2105991370
- Cited by
- 312
- References
- 10
- FWCI
- 10.25
- Type
- journal article
- Language
- en
- Open access
- closed
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