Document Detail


Ghrelin increases the motivation to eat, but does not alter food palatability.
MedLine Citation:
PMID:  22673784     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Homeostatic eating cannot explain overconsumption of food and pathological weight gain. A more likely factor promoting excessive eating is food reward and its representation in the central nervous system (CNS). The anorectic hormones leptin and insulin reduce food reward and inhibit related CNS reward pathways. Conversely, the orexigenic gastrointestinal hormone ghrelin activates both homeostatic and reward-related neurocircuits. The current studies were conducted to identify in rats the effects of intracerebroventricular ghrelin infusions on two distinct aspects of food reward: hedonic valuation (i.e., "liking") and the motivation to self-administer (i.e., "wanting") food. To assess hedonic valuation of liquid food, lick motor patterns were recorded using lickometry. Although ghrelin administration increased energy intake, it did not alter the avidity of licking (initial lick rates or lick-cluster size). Several positive-control conditions ruled out lick-rate ceiling effects. Similarly, when the liquid diet was hedonically devalued with quinine supplementation, ghrelin failed to reverse the quinine-associated reduction of energy intake and avidity of licking. The effects of ghrelin on rats' motivation to eat were assessed using lever pressing to self-administer food in a progressive-ratio paradigm. Ghrelin markedly increased motivation to eat, to levels comparable to or greater than those seen following 24 h of food deprivation. Pretreatment with the dopamine D1 receptor antagonist SCH-23390 eliminated ghrelin-induced increases in lever pressing, without compromising generalized licking motor control, indicating a role for D1 signaling in ghrelin's motivational feeding effects. These results indicate that ghrelin increases the motivation to eat via D1 receptor-dependent mechanisms, without affecting perceived food palatability.
Authors:
Joost Overduin; Dianne P Figlewicz; Jennifer Bennett-Jay; Sepideh Kittleson; David E Cummings
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-06-06
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  303     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-02     Completed Date:  2012-10-16     Revised Date:  2013-08-14    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R259-69     Citation Subset:  IM    
Affiliation:
Veterans Administration Puget Sound Health Care System, Office of Research and Development Medical Research Service, Seattle, Washington, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Benzazepines / pharmacology
Eating / drug effects*,  physiology
Feeding Behavior / drug effects*,  physiology
Food Deprivation / physiology
Ghrelin / administration & dosage,  pharmacology*
Homeostasis / drug effects,  physiology
Infusions, Intraventricular
Male
Models, Animal
Motivation / drug effects*,  physiology
Rats
Rats, Sprague-Dawley
Receptors, Dopamine D1 / antagonists & inhibitors
Grant Support
ID/Acronym/Agency:
DK40963/DK/NIDDK NIH HHS; P30 DK17047/DK/NIDDK NIH HHS; R01 DK089528/DK/NIDDK NIH HHS; R01 DK517498/DK/NIDDK NIH HHS; R01 DK61516/DK/NIDDK NIH HHS; UO1 DK66568/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Benzazepines; 0/Ghrelin; 0/Receptors, Dopamine D1; 0/SCH 23390
Comments/Corrections

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


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