Document Detail

Hypothalamic neuropeptide expression following chronic food restriction in sedentary and wheel-running rats.
MedLine Citation:
PMID:  16216917     Owner:  NLM     Status:  MEDLINE    
When rats are given access to a running-wheel in combination with food restriction, they will become hyperactive and decrease their food intake, a paradoxical phenomenon known as activity-based anorexia (ABA). Little is known about the regulation of the hypothalamic neuropeptides that are involved in the regulation of food intake and energy balance during the development of ABA. Therefore, rats were killed during the development of ABA, before they entered a state of severe starvation. Neuropeptide mRNA expression levels were analysed using quantitative real-time PCR on punches of separate hypothalamic nuclei. As is expected in a state of negative energy balance, expression levels of agouti-related protein (AgRP) and neuropeptide Y (NPY) were increased 5-fold in the arcuate nucleus (ARC) of food-restricted running ABA rats vs 2-fold in sedentary food-restricted controls. The co-regulated expression of AgRP and NPY strongly correlated with relative body weight and white adipose tissue mass. Arcuate expression of pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) was reduced 2-fold in the ABA group. In second-order neurons of the lateral hypothalamic area (LHA), melanin-concentrating hormone (MCH) mRNA expression was upregulated 2-fold in food-restricted running rats, but not in food-restricted sedentary controls. Prepro-orexin, CART and corticotropin-releasing hormone expression levels in the LHA and the paraventricular nucleus (PVN) were unchanged in both food-restricted groups. From this study it was concluded that during the development of ABA, neuropeptides in first-order neurons in the ARC and MCH in the LHA are regulated in an adequate response to negative energy balance, whereas expression levels of the other studied neuropeptides in secondary neurons of the LHA and PVN are unchanged and are probably regulated by factors other than energy status alone.
C E de Rijke; J J G Hillebrand; L A W Verhagen; T A P Roeling; R A H Adan
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of molecular endocrinology     Volume:  35     ISSN:  0952-5041     ISO Abbreviation:  J. Mol. Endocrinol.     Publication Date:  2005 Oct 
Date Detail:
Created Date:  2005-10-11     Completed Date:  2006-01-19     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8902617     Medline TA:  J Mol Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  381-90     Citation Subset:  IM    
Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre Utrecht, Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands.
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MeSH Terms
Adipose Tissue / anatomy & histology,  metabolism
Body Weight
Energy Metabolism*
Food Deprivation*
Hypothalamus / anatomy & histology,  metabolism*
Molecular Sequence Data
Motor Activity / physiology*
Neurons / cytology,  metabolism
Neuropeptides / genetics,  metabolism*
RNA, Messenger / metabolism
Rats, Wistar
Statistics as Topic
Reg. No./Substance:
0/Neuropeptides; 0/RNA, Messenger

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