Document Detail


Circulating GLP-1 and CCK-8 reduce food intake by capsaicin-insensitive, nonvagal mechanisms.
MedLine Citation:
PMID:  22031786     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous reports suggest that glucagon-like peptide (GLP-1), a peptide secreted from the distal small intestine, is an endocrine satiation signal. Nevertheless, there are conflicting reports regarding the site where circulating GLP-1 acts to reduce food intake. To test the hypothesis that vagal afferents are necessary for reduction of food intake by circulating GLP-1, we measured intake of 15% sucrose during intravenous GLP-1 infusion in intact, vagotomized, and capsaicin-treated rats. We also measured sucrose intake during intravenous infusion of cholecystokinin, a peptide known to reduce food intake via abdominal vagal afferents. We found that reduction of intake by GLP-1 was not diminished by capsaicin treatment or vagotomy. In fact, reduction of sucrose intake by our highest GLP-1 dose was enhanced in vagotomized and capsaicin-treated rats. Intravenous GLP-1 induced comparable increases of hindbrain c-Fos immunoreactivity in intact, capsaicin-treated, and vagotomized rats. Plasma concentrations of active GLP-1 in capsaicin-treated rats did not differ from those of controls during the intravenous infusions. Finally, capsaicin treatment was not associated with altered GLP-1R mRNA in the brain, but nodose ganglia GLP-1R mRNA was significantly reduced in capsaicin-treated rats. Although reduction of food intake by intraperitoneal cholecystokinin was abolished in vagotomized and capsaicin-treated rats, reduction of intake by intravenous cholecystokinin was only partially attenuated. These results indicate that vagal or capsaicin-sensitive neurons are not necessary for reduction of food intake by circulating (endocrine) GLP-1, or cholecystokinin. Vagal participation in satiation by these peptides may be limited to paracrine effects exerted near the sites of their secretion.
Authors:
Jingchuan Zhang; Robert C Ritter
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-10-26
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  302     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-04     Completed Date:  2012-02-17     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R264-73     Citation Subset:  IM    
Affiliation:
Programs in Neuroscience and Dept. of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State Univ., Pullman, WA 99164-6520, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain / drug effects,  metabolism
Capsaicin / pharmacology*
Eating / drug effects*,  physiology
Glucagon-Like Peptide 1 / blood,  pharmacology*
Male
Nodose Ganglion / drug effects,  metabolism
Rats
Rats, Sprague-Dawley
Sincalide / blood,  pharmacology*
Vagotomy
Vagus Nerve / drug effects,  physiology*
Grant Support
ID/Acronym/Agency:
DK-52849/DK/NIDDK NIH HHS; NS-20561/NS/NINDS NIH HHS; R01 DK052849/DK/NIDDK NIH HHS; R01 NS020561-27/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
25126-32-3/Sincalide; 404-86-4/Capsaicin; 89750-14-1/Glucagon-Like Peptide 1
Comments/Corrections

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


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