| The diverse roles of specific GLP-1 receptors in the control of food intake and the response to visceral illness. | |
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MedLine Citation:
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PMID: 12451146 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Kimberly P Kinzig; David A D'Alessio; Randy J Seeley |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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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:
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Created Date: 2002-11-26 Completed Date: 2002-12-23 Revised Date: 2013-03-19 |
Medline Journal Info:
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Nlm Unique ID: 8102140 Medline TA: J Neurosci Country: United States |
Other Details:
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Languages: eng Pagination: 10470-6 Citation Subset: IM |
Affiliation:
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Department of Psychiatry, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0559, USA. kinzigkp@emailuc.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Amygdala
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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:
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DK54890/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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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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