RGD Reference Report - Effects of the cannabinoid CB1 antagonist, rimonabant, on hepatic mitochondrial function in rats fed a high fat diet. - Rat Genome Database

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Effects of the cannabinoid CB1 antagonist, rimonabant, on hepatic mitochondrial function in rats fed a high fat diet.

Authors: Flamment, M  Gueguen, N  Wetterwald, C  Simard, G  Malthiery, Y  Ducluzeau, PH 
Citation: Flamment M, etal., Am J Physiol Endocrinol Metab. 2009 Sep 1.
RGD ID: 2314644
Pubmed: PMID:19724020   (View Abstract at PubMed)
DOI: DOI:10.1152/ajpendo.00169.2009   (Journal Full-text)

The aim of this study was to investigate the effect of rimonabant treatment on hepatic mitochondrial function in rats fed a high fat diet. Sprague Dawley rats fed a high fat diet (35% lard) during 13 weeks were treated with rimonabant (10mg/kg/day) during the 3 last weeks and matched with pair-fed controls. Oxygen consumption with various substrates, mitochondrial enzyme activities on isolated liver mitochondria and mitochondrial DNA quantity were determined. Body weight and fat mass were decreased in rats treated with rimonabant compared to pair-fed controls. Moreover, serum adiponectin level was increased with rimonabant. Hepatic triglycerides content was increased while serum triglycerides were decreased. An increase of mitochondrial respiration was observed in rats treated with rimonabant. Especially an increase of mitochondrial respiration with palmitoyl CoA compared to respiration with palmitoyl-l-carnitine stating that the entry of fatty acids into mitochondria via the carnitine palmitoyl transferase I was increased in rats treated with rimonabant. Moreover rimonabant treatment leads to a reduction in the enzymatic activity of the ATP synthase whereas the quantity of mitochondrial DNA and the activity of the citrate synthase were remained unchanged. To summarize, rimonabant treatment leads to an improvement of hepatic mitochondrial function by increasing substrates oxidation and fatty acids entry into mitochondria for the beta-oxidation pathway and by increasing proton leak. However this increase of mitochondrial oxidation is regulated by a decrease of ATP synthase activity in order to have only ATP required to the cell function. Key words: rimonabant, high fat diet, mitochondria, liver, oxidative phosphorylation.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Cnr1Ratnegative regulation of fatty acid beta-oxidation  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Cnr1  (cannabinoid receptor 1)


Additional Information