Document Detail

Reduced hepatic fatty acid oxidation in fasting PPARalpha null mice is due to impaired mitochondrial hydroxymethylglutaryl-CoA synthase gene expression.
MedLine Citation:
PMID:  10869548     Owner:  NLM     Status:  MEDLINE    
Glucose and fatty acid metabolism (oxidation versus esterification) has been measured in hepatocytes isolated from 24 h starved peroxisome proliferator-activated receptor-alpha (PPARalpha) null and wild-type mice. In PPARalpha null mice, the development of hypoglycemia during starvation was due to a reduced capacity for hepatic gluconeogenesis secondary to a 70% lower rate of fatty acid oxidation. This was not due to inappropriate expression of the hepatic CPT I gene, which was similar in both genotypes, but to impaired mitochondrial hydroxymethylglutaryl-CoA synthase gene expression in the PPARalpha null mouse liver. We also demonstrate that hepatic steatosis of fasting PPARalpha null mice was not due to enhanced triglyceride synthesis.
C Le May; T Pineau; K Bigot; C Kohl; J Girard; J P Pégorier
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  FEBS letters     Volume:  475     ISSN:  0014-5793     ISO Abbreviation:  FEBS Lett.     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-07-24     Completed Date:  2000-07-24     Revised Date:  2005-11-17    
Medline Journal Info:
Nlm Unique ID:  0155157     Medline TA:  FEBS Lett     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  163-6     Citation Subset:  IM    
Endocrinologie Métabolisme et Développement, UPR 1524 CNRS, Meudon, France.
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MeSH Terms
Gene Expression Regulation, Enzymologic
Hydroxymethylglutaryl-CoA Synthase / genetics,  metabolism*
Liver / metabolism*
Mice, Knockout
Mitochondria, Liver / genetics,  metabolism
Nuclear Proteins / genetics,  metabolism
Receptors, Cytoplasmic and Nuclear / genetics*,  metabolism*
Transcription Factors / genetics*,  metabolism*
Reg. No./Substance:
0/Nuclear Proteins; 0/Receptors, Cytoplasmic and Nuclear; 0/Transcription Factors; EC Synthase

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