Document Detail


The diverse roles of specific GLP-1 receptors in the control of food intake and the response to visceral illness.
MedLine Citation:
PMID:  12451146     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intracerebroventricular administration of glucagon-like peptide-1 (7-36) amide (GLP-1) reduces food intake and produces symptoms of visceral illness, such as a conditioned taste aversion (CTA). The central hypothesis of the present work is that separate populations of GLP-1 receptors mediate the anorexia and taste aversion associated with GLP-1 administration. To test this hypothesis, we first compared the ability of various doses of GLP-1 to induce anorexia or CTA when administered into either the lateral or fourth ventricle. Lateral and fourth ventricular GLP-1 resulted in reduction of food intake at similar doses, whereas only lateral ventricular GLP-1 resulted in a CTA. Such data indicate that both hypothalamic and caudal brainstem GLP-1 receptors are likely to participate in the ability of GLP-1 to reduce food intake. We also hypothesized that the site that must mediate the ability of GLP-1 to induce visceral illness is in the central nucleus of the amygdala (CeA). Administration of 0.2 or 1.0 microg of GLP-1 (7-36) but not the inactive GLP-1 (9-36) resulted in a strong CTA with no accompanying anorexia. In addition, bilateral CeA administration of 2.5 microg of a GLP-1 receptor antagonist before intraperitoneal administration of the toxin lithium chloride resulted in a diminished CTA. Together, these data indicate that separate GLP-1 receptor populations mediate the multiple responses to GLP-1. These results indicate that GLP-1 is a flexible system that can be activated under various circumstances to alter the ingestion of nutrients and/or produce other visceral illness responses, depending on the ascending pathways of the GLP-1 system that are recruited.
Authors:
Kimberly P Kinzig; David A D'Alessio; Randy J Seeley
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  22     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2002 Dec 
Date Detail:
Created Date:  2002-11-26     Completed Date:  2002-12-23     Revised Date:  2013-03-19    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  10470-6     Citation Subset:  IM    
Affiliation:
Department of Psychiatry, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0559, USA. kinzigkp@emailuc.edu
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MeSH Terms
Descriptor/Qualifier:
Amygdala / drug effects,  physiology
Animals
Anorexia* / chemically induced,  physiopathology
Appetite Regulation / drug effects,  physiology*
Behavior, Animal / drug effects
Catheterization
Conditioning (Psychology) / drug effects
Dose-Response Relationship, Drug
Eating / drug effects
Fourth Ventricle / drug effects
Glucagon
Glucagon-Like Peptide 1
Glucagon-Like Peptides
Injections, Intraperitoneal
Injections, Intraventricular
Lateral Ventricles / drug effects,  physiology
Lithium Chloride / administration & dosage
Male
Paraventricular Hypothalamic Nucleus / drug effects,  physiology
Peptide Fragments / pharmacology
Rats
Rats, Long-Evans
Receptors, Glucagon / antagonists & inhibitors,  metabolism*
Signal Transduction / drug effects,  physiology
Taste / drug effects,  physiology
Visceral Afferents / drug effects,  physiology*
Grant Support
ID/Acronym/Agency:
DK54890/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Peptide Fragments; 0/Receptors, Glucagon; 0/glucagon-like peptide-1 receptor; 119637-73-9/glucagon-like peptide 1 (7-36)amide; 62340-29-8/Glucagon-Like Peptides; 7447-41-8/Lithium Chloride; 89750-14-1/Glucagon-Like Peptide 1; 9007-92-5/Glucagon

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


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