Document Detail


Reward mechanisms in obesity: new insights and future directions.
MedLine Citation:
PMID:  21338878     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Food is consumed in order to maintain energy balance at homeostatic levels. In addition, palatable food is also consumed for its hedonic properties independent of energy status. Such reward-related consumption can result in caloric intake exceeding requirements and is considered a major culprit in the rapidly increasing rates of obesity in developed countries. Compared with homeostatic mechanisms of feeding, much less is known about how hedonic systems in brain influence food intake. Intriguingly, excessive consumption of palatable food can trigger neuroadaptive responses in brain reward circuitries similar to drugs of abuse. Furthermore, similar genetic vulnerabilities in brain reward systems can increase predisposition to drug addiction and obesity. Here, recent advances in our understanding of the brain circuitries that regulate hedonic aspects of feeding behavior will be reviewed. Also, emerging evidence suggesting that obesity and drug addiction may share common hedonic mechanisms will also be considered.
Authors:
Paul J Kenny
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Neuron     Volume:  69     ISSN:  1097-4199     ISO Abbreviation:  Neuron     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-02-22     Completed Date:  2011-04-08     Revised Date:  2014-03-25    
Medline Journal Info:
Nlm Unique ID:  8809320     Medline TA:  Neuron     Country:  United States    
Other Details:
Languages:  eng     Pagination:  664-79     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain / pathology,  physiopathology
Energy Metabolism / physiology*
Feeding Behavior / physiology
Homeostasis / physiology
Humans
Models, Neurological
Obesity / etiology,  psychology*
Reward*
Grant Support
ID/Acronym/Agency:
R01 DA025983-04/DA/NIDA NIH HHS
Comments/Corrections

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


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