Document Detail


Peripheral endocannabinoid dysregulation in obesity: relation to intestinal motility and energy processing induced by food deprivation and re-feeding.
MedLine Citation:
PMID:  19371345     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND PURPOSE: Endocannabinoids in tissues controlling energy homeostasis are altered in obesity, thus contributing to metabolic disorders. Here we evaluate endocannabinoid dysregulation in the small intestine of mice with diet-induced obesity (DIO) and in peripheral tissues of Zucker and lean rats following food deprivation and re-feeding.
EXPERIMENTAL APPROACH: Intestinal transit, evaluated using rhodamine-B-labelled dextran, and small intestinal endocannabinoid levels, measured by liquid chromatography mass spectrometry, were measured in mice fed normal or high-fat diets (HFDs). Endocannabinoid levels were measured also in various tissues of lean and Zucker rats fed ad libitum or following overnight food deprivation with and without subsequent re-feeding.
KEY RESULTS: After 8 weeks of HFD, baseline intestinal transit was increased in DIO mice and enhanced by cannabinoid CB(1) receptor antagonism less efficaciously than in lean mice. Small intestinal anandamide and 2-arachidonoylglycerol levels were reduced and increased respectively. In Zucker rats, endocannabinoids levels were higher in the pancreas, liver and duodenum, and lower in the subcutaneous adipose tissue. Food deprivation increased endocannabinoid levels in the duodenum and liver of both rat strains, in the pancreas of lean rats and in adipose tissues of Zucker rats.
CONCLUSIONS AND IMPLICATIONS: Reduced anandamide levels might account for increased intestinal motility in DIO mice. Regulation of endocannabinoid levels in rat peripheral tissues, induced by food deprivation and re-feeding, might participate in food intake and energy processing and was altered in Zucker rats. These data, together with previous observations, provide further evidence for dysregulation of peripheral endocannabinoids in obesity.
Authors:
Angelo A Izzo; Fabiana Piscitelli; Raffaele Capasso; Gabriella Aviello; Barbara Romano; Francesca Borrelli; Stefania Petrosino; Vincenzo Di Marzo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-04-03
Journal Detail:
Title:  British journal of pharmacology     Volume:  158     ISSN:  1476-5381     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-09-07     Completed Date:  2010-01-05     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  451-61     Citation Subset:  IM    
Affiliation:
Department of Experimental Pharmacology, University of Naples Federico II, Naples, Italy.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arachidonic Acids / metabolism
Cannabinoid Receptor Modulators / metabolism*
Chromatography, Liquid
Endocannabinoids*
Energy Metabolism*
Food Deprivation
Gastrointestinal Motility*
Gastrointestinal Transit
Glycerides / metabolism
Male
Mass Spectrometry
Mice
Mice, Inbred C57BL
Obesity / physiopathology*
Polyunsaturated Alkamides / metabolism
Rats
Rats, Wistar
Rats, Zucker
Receptor, Cannabinoid, CB1 / antagonists & inhibitors,  metabolism
Chemical
Reg. No./Substance:
0/Arachidonic Acids; 0/Cannabinoid Receptor Modulators; 0/Endocannabinoids; 0/Glycerides; 0/Polyunsaturated Alkamides; 0/Receptor, Cannabinoid, CB1; 53847-30-6/2-arachidonylglycerol; 94421-68-8/anandamide
Comments/Corrections

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


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