ArticleThe Biochemical journal2004
Peroxisomal-proliferator-activated receptor alpha activates transcription of the rat hepatic malonyl-CoA decarboxylase gene: a key regulation of malonyl-CoA level.
Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 97 citations in OpenAlex.
- Malonyl-CoA Decarboxylase: A Spotlight on Brain Aspects.Brain sciences · 2026Review
- Advances in myocardial energy metabolism: metabolic remodelling in heart failure and beyond.Cardiovascular research · 2024Review
- Article
- Signal Transduction and Molecular Regulation in Fatty Liver Disease.Antioxidants & redox signaling · 2021Article
- Mechanisms Mediating the Regulation of Peroxisomal Fatty Acid Beta-Oxidation by PPARα.International journal of molecular sciences · 2021Review
- Hepatic transcriptional responses to fasting and feeding.Genes & development · 2021Review
- The Novel Role of PPAR Alpha in the Brain: Promising Target in Therapy of Alzheimer's Disease and Other Neurodegenerative Disorders.Neurochemical research · 2020Review
- Short- and long-term effects of perinatal phthalate exposures on metabolic pathways in the mouse liver.Environmental epigenetics · 2020Article
- Resveratrol Reduces Lipid Accumulation through Upregulating the Expression of MicroRNAs Regulating Fatty Acid Bet Oxidation in Liver Cells: Evidence fromIranian journal of pharmaceutical research : IJPR · 2020Article
- Review
- Pharmacologic activation of peroxisome proliferator-activating receptor-α accelerates hepatic fatty acid oxidation in neonatal pigs.Oncotarget · 2018Article
- PPARα augments heart function and cardiac fatty acid oxidation in early experimental polymicrobial sepsis.American journal of physiology. Heart and circulatory physiology · 2017Article
- Tangshen formula attenuates hepatic steatosis by inhibiting hepatic lipogenesis and augmenting fatty acid oxidation in db/db mice.International journal of molecular medicine · 2016Article
- Protective Effects ofBiomolecules & therapeutics · 2016Article
- Resveratrol and fenofibrate ameliorate fructose-induced nonalcoholic steatohepatitis by modulation of genes expression.World journal of gastroenterology · 2016Article
- Peroxisome Proliferator-Activated Receptor α Protects Renal Tubular Cells from Gentamicin-Induced Apoptosis via Upregulating NaMolecular medicine (Cambridge, Mass.) · 2016Article
- Mechanisms of intrahepatic triglyceride accumulation.World journal of gastroenterology · 2016Review
- Microarray analysis of gene expression in liver, adipose tissue and skeletal muscle in response to chronic dietary administration of NDGA to high-fructose fed dyslipidemic rats.Nutrition & metabolism · 2016Article
- PPARs and Mitochondrial Metabolism: From NAFLD to HCC.PPAR research · 2016Review
- Inhibition of Dexamethasone-induced Fatty Liver Development by Reducing miR-17-5p Levels.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MCD (malonyl-CoA decarboxylase), which catalyses decarboxylation of malonyl-CoA, is known to play an important role in the regulation of malonyl-CoA concentration. Recently, it has been observed that the expression of MCD is significantly decreased in the hearts of the PPARalpha (peroxisome-proliferator-activated receptor alpha) (-/-) mice, where the rate of fatty-acid oxidation is decreased by the increased malonyl-CoA level [Campbell, Kozak, Wagner, Altarejos, Dyck, Belke, Severson, Kelly and Lopaschuk (2002) J. Biol. Chem. 277, 4098-4103]. This suggests that MCD may be transcriptionally regulated by PPARalpha. To investigate whether PPARalpha is truly responsible for transcriptional regulation of the rat MCD gene, transient reporter assay was performed in CV-1 cells. The promoter activity was increased by 17-fold in CV-1 cells co-transfected with PPARalpha/retinoid X receptor alpha expression plasmid. In sequence analysis of the promoter region, three putative PPREs (PPAR response elements) were identified, and promoter deletion analysis showed that PPRE2 and PPRE3 were functional. Electrophoretic mobility-shift assays revealed that PPARalpha/retinoid X receptor alpha heterodimer indeed bound to the two PPREs, and the binding specificity of PPARalpha on PPRE was also confirmed by experiments with mutated oligonucleotides. These results indicate that the elements behaved as a responsive site to PPARalpha activation. MCD mRNA levels in WY14643-treated rat hepatoma cells as well as in the liver of fenofibrate-fed Otsuka Long-Evans Tokushima fatty rats were also found to be increased, suggesting that PPARalpha can activate the rat hepatic MCD transcription by binding to the PPREs in the promoter. We propose that MCD performs an important role in understanding the regulatory mechanism between activated PPARalpha and fatty-acid oxidation by altering the malonyl-CoA concentration.
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