| The role of nausea in food intake and body weight suppression by peripheral GLP-1 receptor agonists, exendin-4 and liraglutide. | |
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MedLine Citation:
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PMID: 22227019 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The FDA-approved glucagon-like-peptide-1 receptor (GLP-1R) agonists exendin-4 and liraglutide reduce food intake and body weight. Nausea is the most common adverse side effect reported with these GLP-1R agonists. Whether food intake suppression by exendin-4 and liraglutide occurs independently of nausea is unknown. Further, the neurophysiological mechanisms mediating the nausea associated with peripheral GLP-1R agonist use are poorly understood. Using two established rodent models of nausea [conditioned taste avoidance (CTA) and pica (ingestion of nonnutritive substances)], results show that all peripheral doses of exendin-4 that suppress food intake also produce CTA, whereas one dose of liraglutide suppresses intake without producing CTA. Chronic (12 days) daily peripheral administration of exendin-4 produces a progressive increase in pica coupled with stable, sustained food intake and body weight suppression, whereas the pica response and food intake reduction by daily liraglutide are more transient. Results demonstrate that the nausea response accompanying peripheral exendin-4 occurs via a vagal-independent pathway involving GLP-1R activation in the brain as the exendin-4-induced pica response is attenuated with CNS co-administration of the GLP-1R antagonist exendin-(9-39), but not by vagotomy. Direct administration of exendin-4 to the medial subnucleus of the nucleus tractus solitarius (mNTS), but not to the central nucleus of the amygdala, reduced food intake and produced a pica response, establishing the mNTS as a potential GLP-1R-expressing site mediating nausea responses associated with GLP-1R agonists. |
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Authors:
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Scott E Kanoski; Laura E Rupprecht; Samantha M Fortin; Bart C De Jonghe; Matthew R Hayes |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-12-28 |
Journal Detail:
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Title: Neuropharmacology Volume: 62 ISSN: 1873-7064 ISO Abbreviation: Neuropharmacology Publication Date: 2012 Apr |
Date Detail:
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Created Date: 2012-02-13 Completed Date: 2012-07-23 Revised Date: 2013-05-13 |
Medline Journal Info:
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Nlm Unique ID: 0236217 Medline TA: Neuropharmacology Country: England |
Other Details:
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Languages: eng Pagination: 1916-27 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Psychology, School of Art and Science, University of Pennsylvania, Philadelphia, PA 19104, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Body Weight / drug effects*, physiology Eating / drug effects*, physiology Glucagon-Like Peptide 1 / analogs & derivatives*, toxicity Hypoglycemic Agents / toxicity* Male Nausea / chemically induced*, physiopathology Peptides / toxicity* Rats Rats, Sprague-Dawley Receptors, Glucagon / agonists* Solitary Nucleus / drug effects, physiopathology Vagus Nerve / drug effects, physiopathology Venoms / toxicity* |
| Grant Support | |
ID/Acronym/Agency:
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DK085435/DK/NIDDK NIH HHS; DK089752/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Hypoglycemic Agents; 0/Peptides; 0/Receptors, Glucagon; 0/Venoms; 0/glucagon-like peptide-1 receptor; 141732-76-5/exenatide; 839I73S42A/liraglutide; 89750-14-1/Glucagon-Like Peptide 1 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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