Document Detail


Hypothalamic signaling in anorexia induced by indispensable amino acid deficiency.
MedLine Citation:
PMID:  23047987     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Animals exhibit a rapid and sustained anorexia when fed a diet that is deficient in a single indispensable amino acid (IAA). The chemosensor for IAA deficiency resides within the anterior piriform cortex (APC). Although the cellular and molecular mechanisms by which the APC detects IAA deficiency are well established, the efferent neural pathways that reduce feeding in response to an IAA-deficient diet remain to be fully characterized. In the present work, we investigated whether 1) central melanocortin signaling is involved in IAA deficiency-induced anorexia (IAADA) and 2) IAADA engages other key appetite-regulating neuronal populations in the hypothalamus. Rats and mice that consumed a valine-deficient diet (VDD) for 2-3 wk exhibited marked reductions in food intake, body weight, fat and lean body mass, body temperature, and white adipose tissue leptin gene expression, as well as a paradoxical increase in brown adipose tissue uncoupling protein-1 mRNA. Animals consuming the VDD had altered hypothalamic gene expression, typical of starvation. Pharmacological and genetic blockade of central melanocortin signaling failed to increase long-term food intake in this model. Chronic IAA deficiency was associated with a marked upregulation of corticotropin-releasing hormone expression in the lateral hypothalamus, particularly in the parasubthalamic nucleus, an area heavily innervated by efferent projections from the APC. Our observations indicate that the hypothalamic melanocortin system plays a minor role in acute, but not chronic, IAADA and suggest that the restraint on feeding is analogous to that observed after chronic dehydration.
Authors:
Xinxia Zhu; Stephanie M Krasnow; Quinn R Roth-Carter; Peter R Levasseur; Theodore P Braun; Aaron J Grossberg; Daniel L Marks
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-10-09
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  303     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-17     Completed Date:  2013-02-25     Revised Date:  2013-12-18    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E1446-58     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue, Brown / metabolism
Adipose Tissue, White / metabolism
Animals
Anorexia / etiology*,  metabolism*,  pathology
Corticotropin-Releasing Hormone / genetics,  metabolism
Female
Gene Expression Regulation
Hypothalamus / metabolism*,  pathology
Ion Channels / genetics,  metabolism
Leptin / genetics,  metabolism
Male
Melanocortins / metabolism
Mice
Mice, Knockout
Mitochondrial Proteins / genetics,  metabolism
Neural Pathways / metabolism*,  pathology
Neurons / metabolism*,  pathology
Organ Specificity
Rats
Rats, Sprague-Dawley
Receptor, Melanocortin, Type 4 / genetics,  metabolism
Signal Transduction*
Valine / deficiency*,  metabolism
Grant Support
ID/Acronym/Agency:
DK-070333/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Ion Channels; 0/Leptin; 0/MC4R protein, mouse; 0/Melanocortins; 0/Mitochondrial Proteins; 0/Receptor, Melanocortin, Type 4; 0/mitochondrial uncoupling protein; 9015-71-8/Corticotropin-Releasing Hormone; HG18B9YRS7/Valine
Comments/Corrections

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


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