Document Detail


Obesogenic diets may differentially alter dopamine control of sucrose and fructose intake in rats.
MedLine Citation:
PMID:  21549729     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic overeating of obesogenic diets can lead to obesity, reduced dopamine signaling, and increased consumption of added sugars to compensate for blunted reward. However, the specific role of diet composition yet remains unknown. To study this, Sprague-Dawley male rats were fed a high-energy diet with high fat and low carbohydrate content (HFHE), a fat-sugar combination high-energy diet (FCHE), or standard chow for 24 weeks. We found that both high-energy diets produced substantial body weight gain compared to chow-fed controls. To investigate dopamine control of short (2-h) intake of palatable sucrose or fructose solutions, rats were pretreated peripherally (IP) with equimolar doses (0-600 nmol/kg) of the dopamine D1 (SCH23390) and D2 (raclopride) subtype-specific receptor antagonists. The results showed an overall increase in the efficacy of D1 and D2 receptor antagonists on suppression of intake in obese rats compared to lean rats, with effects differing based on diets and test solutions. Specifically, SCH23390 potently reduced both sucrose and fructose intake in all groups; however, lower doses were more effective in HFHE rats. In contrast, raclopride was most effective at reducing fructose intake in the obese FCHE rats. Thus, it appears that obesity due to the consumption of combinations of dietary fat and sugar rather than extra calories from dietary fat alone may result in reduced D2 receptor signaling. Furthermore, such deficits seem to preferentially affect the control of fructose intake. These findings demonstrate for the first time a plausible interaction between diet composition and dopamine control of carbohydrate intake in diet-induced obese rats. It also provides additional evidence that sucrose and fructose intake is regulated differentially by the dopamine system.
Authors:
Carolyn E Pritchett; Andras Hajnal
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-05-01
Journal Detail:
Title:  Physiology & behavior     Volume:  104     ISSN:  1873-507X     ISO Abbreviation:  Physiol. Behav.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-06-03     Completed Date:  2011-10-14     Revised Date:  2012-02-14    
Medline Journal Info:
Nlm Unique ID:  0151504     Medline TA:  Physiol Behav     Country:  United States    
Other Details:
Languages:  eng     Pagination:  111-6     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Affiliation:
Pennsylvania State University College of Medicine, The Milton S. Hershey Medical Center, Department of Neural and Behavioral Sciences, Hershey, PA 17033, United States.
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MeSH Terms
Descriptor/Qualifier:
Adiposity / physiology*
Animals
Body Weight / drug effects,  physiology
Dietary Fats / administration & dosage
Dopamine / metabolism*
Dopamine Antagonists / pharmacology
Eating / drug effects,  physiology*
Energy Intake / drug effects,  physiology
Fructose / administration & dosage*
Male
Obesity / metabolism*,  physiopathology
Raclopride / pharmacology
Rats
Rats, Sprague-Dawley
Sucrose / administration & dosage*
Grant Support
ID/Acronym/Agency:
DC000240/DC/NIDCD NIH HHS; DK080899/DK/NIDDK NIH HHS; R01 DC000240-29/DC/NIDCD NIH HHS; R01 DC000240-30/DC/NIDCD NIH HHS; R01 DK080899-03/DK/NIDDK NIH HHS; R01 DK080899-04/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Dietary Fats; 0/Dopamine Antagonists; 30237-26-4/Fructose; 57-50-1/Sucrose; 84225-95-6/Raclopride

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


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