Document Detail

The role of the vagus nerve in mediating the long-term anorectic effects of leptin.
MedLine Citation:
PMID:  17355316     Owner:  NLM     Status:  MEDLINE    
Leptin, the product of the obese (ob) gene, is mainly known for its regulatory role of energy balance by direct activation of hypothalamic receptors. Recently, its function in the acute control of food intake was additionally attributed to activation of the vagus nerve to regulate meal termination. Whether vagal afferent neurones are involved in longer term effects of leptin on food intake, however, remains undetermined. Using vagotomised (VGX) rats, we sought to clarify the contributions of vagal afferents in mediating the long-lasting effect of leptin on appetite suppression. Intraperitoneal (i.p.) injection of leptin (3.5 mg/kg) attenuated food intake at 4, 6, 8 and 24 h and body weight at 24 h postinjection in SHAM-operated rats; however, this response was not abrogated by vagotomy. In a separate study using immunohistochemistry, we observed leptin-induced Fos expression in the nucleus tractus solitarii, a brain structure where vagal afferent fibres terminate. This signal was not attenuated in VGX animals compared to the SHAM group. Moreover, leptin treatment led to a similar level of nuclear STAT3 translocation, a marker of leptin signalling, in the hypothalami of SHAM and VGX animals. In addition to the effects of leptin, vagotomy surgery itself resulted in a decrease of 24 h food intake. Analyses of brains from saline-treated VGX animals revealed a significant induction of Fos in the nucleus tractus solitarii and changes in agouti-related peptide and pro-opiomelanocortin mRNA expression in the hypothalamus compared to their SHAM counterparts, indicating that the vagotomy surgery itself induced a modification of brain activity in areas involved in regulating appetite. Collectively, our data suggest that vagal afferents do not constitute a major route of mediating the regulatory effect of leptin on food intake over a period of several hours.
C Sachot; C Rummel; A F Bristow; G N Luheshi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neuroendocrinology     Volume:  19     ISSN:  0953-8194     ISO Abbreviation:  J. Neuroendocrinol.     Publication Date:  2007 Apr 
Date Detail:
Created Date:  2007-03-14     Completed Date:  2007-05-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8913461     Medline TA:  J Neuroendocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  250-61     Citation Subset:  IM    
Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Montreal, Quebec, Canada.
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MeSH Terms
Anorexia / metabolism*
Appetite Regulation / physiology*
Eating / physiology
Hypothalamus / metabolism
Leptin / physiology*
Neurons, Afferent / physiology
Proto-Oncogene Proteins c-fos / metabolism
Rats, Sprague-Dawley
STAT3 Transcription Factor / metabolism
Signal Transduction / physiology
Solitary Nucleus / metabolism*
Vagus Nerve / cytology,  physiology*
Reg. No./Substance:
0/Leptin; 0/Proto-Oncogene Proteins c-fos; 0/STAT3 Transcription Factor

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

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