| Gastrointestinal satiety signals. | |
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MedLine Citation:
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PMID: 17937600 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The increasing prevalence of obesity worldwide has imparted renewed impetus to the study of the mechanisms of appetite regulation. Digestion and nutrient absorption take place in the gastrointestinal (GI) tract, whereas food intake is controlled by neuronal circuits in the central nervous system. The need for gut-brain cross talk is therefore clear. It is now recognized that hormones released into the circulation from the GI tract in response to nutritional stimuli form a key component of this gut-brain axis. Peptides such as glucagon-like peptide-1, oxyntomodulin, pancreatic polypeptide, and peptide YY3-36 reduce food intake in both animal models and in humans. Physiologically, such peptides are thought to act as satiety signals and meal terminators. Here, we review the current state of the field of the effects of gut hormone action on appetite control. |
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Authors:
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Owais B Chaudhri; Victoria Salem; Kevin G Murphy; Stephen R Bloom |
Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Annual review of physiology Volume: 70 ISSN: 0066-4278 ISO Abbreviation: Annu. Rev. Physiol. Publication Date: 2008 |
Date Detail:
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Created Date: 2008-02-14 Completed Date: 2008-05-16 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0370600 Medline TA: Annu Rev Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 239-55 Citation Subset: IM |
Affiliation:
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Department of Metabolic Medicine, Imperial College London, Hammersmith Hospital, London W12 0NN, United Kingdom. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Enteric Nervous System / physiology* Gastrointestinal Hormones / metabolism* Gastrointestinal Tract / innervation, physiology* Humans Satiety Response / physiology* Signal Transduction / physiology* Vagus Nerve / physiology |
| Chemical | |
Reg. No./Substance:
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0/Gastrointestinal Hormones |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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