scholarly journals Fatty Acids Activate Transcription of the Muscle Carnitine Palmitoyltransferase I Gene in Cardiac Myocytes via the Peroxisome Proliferator-activated Receptor α

1998 ◽  
Vol 273 (37) ◽  
pp. 23786-23792 ◽  
Author(s):  
Jon M. Brandt ◽  
Fatima Djouadi ◽  
Daniel P. Kelly
Keyword(s):  
Fatty Acids ◽  
Cardiac Myocytes ◽  
Carnitine Palmitoyltransferase ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Carnitine Palmitoyltransferase I ◽  
I Gene

Long-chain fatty acids regulate liver carnitine palmitoyltransferase I gene (L-CPT I) expression through a peroxisome-proliferator-activated receptor α (PPARα)-independent pathway

2001 ◽  
Vol 354 (1) ◽  
pp. 189-197 ◽  
Author(s):  
Jean-Francç;ois LOUET ◽  
Florence CHATELAIN ◽  
Jean-Francç;ois DECAUX ◽  
Edwards A. PARK ◽  
Claude KOHL ◽  
...  
Keyword(s):  
Gene Expression ◽  
Carnitine Palmitoyltransferase ◽  
Dietary Lipids ◽  
Lipid Lowering ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Carnitine Palmitoyltransferase I ◽  
Cpt I ◽  
I Gene ◽  
Long Chain

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 α (PPARα) 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 PPARα-null mice. These results suggest that the PPARα-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 PPARα-independent pathways and suggest that the regulation of gene expression by dietary lipids is more complex than previously proposed.

Regulation of liver carnitine palmitoyltransferase I gene expression by hormones and fatty acids

2001 ◽  
Vol 29 (2) ◽  
pp. 310-316 ◽  
Author(s):  
J.-F. Louet ◽  
C. Le May ◽  
J.-P. Pégorier ◽  
J.-F. Decaux ◽  
J. Girard
Keyword(s):  
Fatty Acids ◽  
Gene Transcription ◽  
Peroxisome Proliferator ◽  
Gene Encoding ◽  
First Intron ◽  
Transcriptional Effect ◽  
Carnitine Palmitoyltransferase I ◽  
Responsive Element ◽  
Cpt I ◽  
I Gene

This brief review focuses on the transcriptional regulation of liver carnitine palmitoyltransferase I (L-CPT I) by pancreatic and thyroid hormones and by long-chain fatty acids (LCFA). Both glucagon and 3,3′,5-tri-iodothyronine (T3) enhanced the transcription of the gene encoding L-CPT I, whereas insulin had the opposite effect. Interestingly, the transcriptional effect of T3 required, in addition to the thyroid-responsive element, the co-operation of a sequence located in the first intron of L-CPT I gene. Non-esterified fatty acids rather than acyl-CoA ester or intramitochondrial metabolite were responsible for the transcriptional effect on the gene encoding LCPT I. It was shown that LCFA and peroxisome proliferators stimulated L-CPT I gene transcription by distinct mechanisms. Peroxisome proliferator stimulated L-CPT I gene transcription through a peroxisome-proliferator-responsive element (PPRE) located at -2846 bp, whereas LCFA induced L-CPT I gene transcription through a peroxisome-proliferator-activated receptor α (PPARα)-independent mechanism owing to a sequence located in the first intron of the gene.

Cyclic AMP and Fatty Acids Increase Carnitine Palmitoyltransferase I Gene Transcription in Cultured Fetal Rat Hepatocytes

1996 ◽  
Vol 235 (3) ◽  
pp. 789-798 ◽  
Author(s):  
Florence Chatelain ◽  
Claude Kohl ◽  
Victoria Esser ◽  
J. Denis Mcgarry ◽  
Jean Girard ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cyclic Amp ◽  
Gene Transcription ◽  
Rat Hepatocytes ◽  
Carnitine Palmitoyltransferase ◽  
Fetal Rat ◽  
Carnitine Palmitoyltransferase I ◽  
I Gene

scholarly journals Fatty Acids Rapidly Induce the Carnitine Palmitoyltransferase I Gene in the Pancreatic β-Cell Line INS-1

1997 ◽  
Vol 272 (3) ◽  
pp. 1659-1664 ◽  
Author(s):  
Fran¸oise Assimacopoulos-Jeannet ◽  
Stéphane Thumelin ◽  
Enrique Roche ◽  
Victoria Esser ◽  
J. Denis McGarry ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cell Line ◽  
Carnitine Palmitoyltransferase ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Carnitine Palmitoyltransferase I ◽  
I Gene

scholarly journals Polymorphism and Human Health

PPAR Research ◽  
2009 ◽  
Vol 2009 ◽  
pp. 1-15 ◽  
Author(s):  
Weimin He
Keyword(s):  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Unsaturated Fatty Acids ◽  
Polycystic Ovary ◽  
Human Subjects ◽  
Saturated Fatty Acids ◽  
Nuclear Hormone Receptor ◽  
Peroxisome Proliferator ◽  
Pro12ala Polymorphism ◽  
Peroxisome Proliferator Activated Receptor

The nuclear hormone receptor peroxisome proliferator activated receptor gamma (PPAR) is an important transcription factor regulating adipocyte differentiation, lipid and glucose homeostasis, and insulin sensitivity. Numerous genetic mutations of PPAR have been identified and these mutations positively or negatively regulate insulin sensitivity. Among these, a relatively common polymorphism of PPAR, Pro12Ala of PPAR2, the isoform expressed only in adipose tissue has been shown to be associated with lower body mass index, enhanced insulin sensitivity, and resistance to the risk of type 2 diabetes in human subjects carrying this mutation. Subsequent studies in different ethnic populations, however, have revealed conflicting results, suggesting a complex interaction between the PPAR2 Pro12Ala polymorphism and environmental factors such as the ratio of dietary unsaturated fatty acids to saturated fatty acids and/or between the PPAR2 Pro12Ala polymorphism and genetic factors such as polymorphic mutations in other genes. In addition, this polymorphic mutation in PPAR2 is associated with other aspects of human diseases, including cancers, polycystic ovary syndrome, Alzheimer disease and aging. This review will highlight findings from recent studies.

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