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rdf:type |
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lifeskim:mentions |
umls-concept:C0015684,
umls-concept:C0017262,
umls-concept:C0017337,
umls-concept:C0085862,
umls-concept:C0166415,
umls-concept:C0185117,
umls-concept:C0597357,
umls-concept:C0851285,
umls-concept:C1299583,
umls-concept:C1413688,
umls-concept:C1549571,
umls-concept:C1608386,
umls-concept:C1704259,
umls-concept:C1705987,
umls-concept:C2003941,
umls-concept:C2911684
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pubmed:issue |
Pt 1
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pubmed:dateCreated |
2001-2-22
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pubmed:abstractText |
Liver carnitine palmitoyltransferase I (L-CPT I) catalyses the transfer of long-chain fatty acid (LCFA) for translocation across the mitochondrial membrane. Expression of the L-CPT I gene is induced by LCFAs as well as by lipid-lowering compounds such as clofibrate. Previous studies have suggested that the peroxisome-proliferator-activated receptor alpha (PPARalpha) is a common mediator of the transcriptional effects of LCFA and clofibrate. We found that free LCFAs rather than acyl-CoA esters are the signal metabolites responsible for the stimulation of L-CPT I gene expression. Using primary culture of hepatocytes we found that LCFAs failed to stimulate L-CPT I gene expression both in wild-type and PPARalpha-null mice. These results suggest that the PPARalpha-knockout mouse does not represent a suitable model for the regulation of L-CPT I gene expression by LCFAs in the liver. Finally, we determined that clofibrate stimulates L-CPT I through a classical direct repeat 1 (DR1) motif in the promoter of the L-CPT I gene while LCFAs induce L-CPT I via elements in the first intron of the gene. Our results demonstrate that LCFAs can regulate gene expression through PPARalpha-independent pathways and suggest that the regulation of gene expression by dietary lipids is more complex than previously proposed.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11171094-10051425,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11171094-9830040
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
|
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0264-6021
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pubmed:author |
|
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
354
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
189-97
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