Document Detail


Interactions between gastric emptying and satiety, with special reference to glucagon-like peptide-1.
MedLine Citation:
PMID:  11790437     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The slowing of gastric emptying is an important mechanism for the satiating effect of gut peptide signaling. After food intake, cholecystokinin (CCK), as well as glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-2 (GLP-2), are released from the gastrointestinal tract to mediate satiety. In humans, CCK and the GLP-1 have been found to cause satiety in both normal and obese subjects. This satiating effect may be caused by the peptides circulating as hormones with direct effects in the central nervous system, or indirect effects through signals mediated either via the vagus nerve or by activation of vagal afferent fibers due to slow gastric emptying. These peptides also cause gastric relaxation, considered an additional component in the satiating effect of the peptides. To conclude, after food intake, gut peptides may act in concert as neurohormonal satiety signals acting directly in the brain or indirectly via the vagus nerve, as well as through gastric sensory mechanisms to limit food intake.
Authors:
P M Hellström; E Näslund
Related Documents :
12630607 - The magenstrasse and mill operation for morbid obesity.
6279467 - Quantification of the fate of dietary fiber in humans by a newly developed radiolabeled...
23229307 - The effects of amphetamine injections on feeding behavior and the brain expression of o...
18270777 - Laparoscopic sleeve gastrectomy with ileal transposition (sgit): a new surgical procedu...
18996877 - Association of breakfast energy density with diet quality and body mass index in americ...
3560877 - Variation of lumbar spine stiffness with load.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Physiology & behavior     Volume:  74     ISSN:  0031-9384     ISO Abbreviation:  Physiol. Behav.     Publication Date:    2001 Nov-Dec
Date Detail:
Created Date:  2002-01-15     Completed Date:  2002-03-07     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0151504     Medline TA:  Physiol Behav     Country:  United States    
Other Details:
Languages:  eng     Pagination:  735-41     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, Unit of Gastroenterology Karolinska Hospital, Karolinska Institutet, SE-171 76, Stockholm, Sweden. per.hellstrom@medks.ki.se
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Body Weight / physiology
Cholecystokinin / physiology
Eating / physiology*
Gastric Emptying / physiology*
Glucagon / physiology*
Glucagon-Like Peptide 1
Glucagon-Like Peptide 2
Humans
Obesity / physiopathology
Peptide Fragments / physiology*
Peptides / physiology
Protein Precursors / physiology*
Satiety Response / physiology*
Vagus Nerve / physiopathology
Chemical
Reg. No./Substance:
0/Glucagon-Like Peptide 2; 0/Peptide Fragments; 0/Peptides; 0/Protein Precursors; 89750-14-1/Glucagon-Like Peptide 1; 9007-92-5/Glucagon; 9011-97-6/Cholecystokinin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Oral, gastric and intestinal influences on human feeding.
Next Document:  Gastric capacity in normal, obese, and bulimic women.