Document Detail


Feeding and reward: ontogenetic changes in an animal model of obesity.
MedLine Citation:
PMID:  22401956     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Given that food is a natural reinforcement, deficits in the reward system can lead to disordered eating behavior, inducing or worsening an already existing pre-obese phenotype. In order to evaluate developmental, food-reward-related measures we used the OLETF rat, an animal model of early-onset overeating-induced obesity, and a natural CCK-1 receptor knockout. Dopamine-like-receptor type 1 (D1R) and D2R levels were examined in a reward-related brain area (Nac shell) and sucrose preference was assessed at selected time points from weaning to adulthood (postnatal day [PND]90). In addition, a group of OLETF was pair fed (PF) to the amount of food consumed by same-age LETO controls (from weaning to PND 90) to examine the contribution of overweight to the alteration in DR expression. In addition, we examined food "craving"-like behavior by analyzing microstructural patterns of licking a palatable liquid diet. OLETF rats expressed significantly lower D2R levels than LETO controls only on PND 90. In PF OLETF, weight and D2R levels were normalized. In addition, OLETF presented exaggerated preference for the high sucrose concentration. After 30-day abstinence, OLETF rats presented significant increased initial rate of licking, suggesting food "craving". Thus, adult OLETF rats demonstrated altered D2R signaling similar to drug-induced sensitization, suggesting a link with their avidity for sucrose and their abnormal craving response. However, the current findings of a late deficit appearance and the novel PF results suggest that deficits in the motivation/regulatory systems of the OLETF rat are a developing process (at least from weaning and on) depending on the overeating and obese phenotype of the rats and not only on the CCK mutation.
Authors:
Asaf Marco; Mariana Schroeder; Aron Weller
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-03-01
Journal Detail:
Title:  Neuropharmacology     Volume:  62     ISSN:  1873-7064     ISO Abbreviation:  Neuropharmacology     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-04-16     Completed Date:  2012-08-10     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  0236217     Medline TA:  Neuropharmacology     Country:  England    
Other Details:
Languages:  eng     Pagination:  2447-54     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Ltd. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Body Weight / physiology*
Disease Models, Animal
Eating / physiology
Feeding Behavior / physiology*
Hyperphagia / genetics,  metabolism*
Nucleus Accumbens / metabolism*
Obesity / genetics,  metabolism*
Rats
Rats, Inbred OLETF
Receptor, Cholecystokinin A / genetics,  metabolism
Receptors, Dopamine D1 / genetics,  metabolism
Receptors, Dopamine D2 / genetics,  metabolism
Reward
Grant Support
ID/Acronym/Agency:
R01 DK057609/DK/NIDDK NIH HHS; R01 DK057609-10/DK/NIDDK NIH HHS; R01 DK57609/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Receptor, Cholecystokinin A; 0/Receptors, Dopamine D1; 0/Receptors, Dopamine D2
Comments/Corrections

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


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