Document Detail


Hyperphagia induced by sucrose: relation to circulating and CSF glucose and corticosterone and orexigenic peptides in the arcuate nucleus.
MedLine Citation:
PMID:  21036188     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Sucrose-rich diets compared to starch-rich diets are known to stimulate overeating under chronic conditions. The present study in normal-weight rats established an acute "preload-to-test meal" paradigm for demonstrating sucrose-induced hyperphagia and investigating possible mechanisms that mediate this behavioral phenomenon. In this acute paradigm, the rats were first given a small (15 kcal) sucrose preload (30% sucrose) for 30 min compared to an equicaloric, starch preload (25% starch with 5% sucrose) and then allowed to freely consume a subsequent test meal of lab chow. The sucrose preload, when compared to a starch preload equal in energy density and palatability, consistently increased food intake in the subsequent test meal occurring between 60 and 120 min after the end of the preload. Measurements of hormones, metabolites and hypothalamic peptides immediately preceding this hyperphagia revealed marked differences between the sucrose vs starch groups that could contribute to the increase in food intake. Whereas the sucrose group compared to the starch group immediately after the preload (at 10 min) had elevated levels of glucose in serum and cerebrospinal fluid (CSF) along with reduced expressions of neuropeptide Y (NPY) and agouti-related protein (AgRP) in the arcuate nucleus (ARC), the subsequent effects (at 30-60 min) just preceding the test meal hyperphagia were the reverse. Along with lower levels of glucose, they included markedly elevated serum and CSF levels of corticosterone and mRNA levels of NPY and AgRP in the ARC. In addition to establishing an animal model for sucrose-induced hyperphagia, these results demonstrate peripheral and central mechanisms that may mediate this behavioral phenomenon.
Authors:
V A Gaysinskaya; O Karatayev; J Shuluk; S F Leibowitz
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-10-29
Journal Detail:
Title:  Pharmacology, biochemistry, and behavior     Volume:  97     ISSN:  1873-5177     ISO Abbreviation:  Pharmacol. Biochem. Behav.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-14     Completed Date:  2011-04-11     Revised Date:  2012-01-04    
Medline Journal Info:
Nlm Unique ID:  0367050     Medline TA:  Pharmacol Biochem Behav     Country:  United States    
Other Details:
Languages:  eng     Pagination:  521-30     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Affiliation:
The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arcuate Nucleus / metabolism*
Base Sequence
Corticosterone / metabolism*
DNA Primers
Hyperphagia / chemically induced*
In Situ Hybridization
Male
Peptides / metabolism*
Polymerase Chain Reaction
Rats
Rats, Sprague-Dawley
Sucrose / adverse effects*
Grant Support
ID/Acronym/Agency:
DA21518/DA/NIDA NIH HHS; R01 DA021518-20/DA/NIDA NIH HHS
Chemical
Reg. No./Substance:
0/DNA Primers; 0/Peptides; 50-22-6/Corticosterone; 57-50-1/Sucrose

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