Document Detail


The endocannabinoid system: a new target for the regulation of energy balance and metabolism.
MedLine Citation:
PMID:  17667864     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent studies have provided evidence that the endocannabinoid (EC) system has very significant effects on energy balance and metabolism through the central control of appetite and by affecting peripheral metabolism. Endocannabinoids are endogenous phospholipid derivatives which bind and activate cannabinoid receptors type 1 and type 2 (CB1 and CB2 receptors). The CB1 receptor, a G-protein coupled receptor, is believed to be responsible for the majority of the central effects of endocannaboids on appetite. Chronic positive energy balance and obesity have been associated with an overactivation of the endocannaboid system which has been suggested to contribute to the development of abdominal obesity and to associated metabolic abnormalities which increase the risk of cardiovascular disease and type 2 diabetes. Animal studies had shown that stimulation of the cannabinoid CB1 receptor with endocannaboids such as anandamide could induce first an increase in food intake leading to body weight gain. Furthermore, an exciting development in this field has been the discovery of CB1 receptors in many peripheral tissues, including key organs involved in carbohydrate and lipid metabolism such as the adipose tissue and liver. Thus, blocking CB1 receptors located in the liver and adipose tissue could have an additional impact on the metabolic risk profile beyond what could be explained by the reduction in food intake and the related body weight loss. Preclinical studies have shown that rimonabant, the first CB1-receptor blocker to be available in clinical practice, could not only induce a reduction in food intake, but could also produce body weight loss beyond what could be explained by its effect on food intake. Thus, the evidence from preclinical studies have suggested that CB1 blockade could represent a relevant approach to reduce food intake, to induce body weight loss, and, most importantly, to "fix" the dysmetabolic state of viscerally obese patients at increased cardiometabolic risk.
Authors:
Jean-Pierre Després
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Critical pathways in cardiology     Volume:  6     ISSN:  1535-2811     ISO Abbreviation:  Crit Pathw Cardiol     Publication Date:  2007 Jun 
Date Detail:
Created Date:  2007-08-01     Completed Date:  2007-09-19     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  101165286     Medline TA:  Crit Pathw Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  46-50     Citation Subset:  IM    
Affiliation:
Québec Heart Institute, Québec QC, Canada. jean-pierre.despres@crhl.ulaval.ca
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MeSH Terms
Descriptor/Qualifier:
Adipocytes / metabolism
Adiponectin / metabolism
Animals
Appetite Regulation / drug effects*
Arachidonic Acids / pharmacology
Carbohydrate Metabolism / drug effects,  physiology
Diabetes Mellitus, Type 2 / prevention & control
Eating / drug effects*
Endocannabinoids / metabolism*
Energy Metabolism / drug effects*
Humans
Lipid Metabolism / drug effects,  physiology
Obesity / prevention & control
Piperidines / pharmacology*
Polyunsaturated Alkamides / pharmacology
Pyrazoles / pharmacology*
Randomized Controlled Trials as Topic
Receptor, Cannabinoid, CB1 / agonists,  antagonists & inhibitors
Tetrahydrocannabinol / pharmacology
Chemical
Reg. No./Substance:
0/Adiponectin; 0/Arachidonic Acids; 0/Endocannabinoids; 0/Piperidines; 0/Polyunsaturated Alkamides; 0/Pyrazoles; 0/Receptor, Cannabinoid, CB1; 158681-13-1/rimonabant; 1972-08-3/Tetrahydrocannabinol; 94421-68-8/anandamide

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


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