A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.

@article{Fidaleo2011ARF,
  title={A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPAR$\alpha$-mediated upregulation of SREBP-2 target genes in the liver.},
  author={Marco Fidaleo and S{\'e}gol{\`e}ne Arnauld and M. C. Cl{\'e}mencet and Gr{\'e}gory Chevillard and Marie-Charlotte Royer and Melina De Bruycker and Ronald J.A. Wanders and Anne Athias and Joseph Gresti and Pierre Clouet and P. Passilly Degrace and Sander Kersten and Marc F. Espeel and Norbert Latruffe and Val{\'e}rie Nicolas-Franc{\'e}s and St{\'e}phane Mandard},
  journal={Biochimie},
  year={2011},
  volume={93 5},
  pages={
          876-91
        }
}
Murine deficiency of peroxisomal L-bifunctional protein (EHHADH) causes medium-chain 3-hydroxydicarboxylic aciduria and perturbs hepatic cholesterol homeostasis
TLDR
It is concluded that EHHADH plays an essential role in the metabolism of medium-chain DCAs and postulate that peroxisomal DCA β-oxidation is a regulator of hepatic cholesterol biosynthesis.
Murine deficiency of peroxisomal L-bifunctional protein (EHHADH) causes medium-chain 3-hydroxydicarboxylic aciduria and perturbs hepatic cholesterol homeostasis.
TLDR
It is concluded that EHHADH plays an essential role in the metabolism of medium-chain DCAs and postulate that peroxisomal DCA β-oxidation is a regulator of hepatic cholesterol biosynthesis.
Human Peroxisomal 3-Ketoacyl-CoA Thiolase: Tissue Expression and Metabolic Regulation : Human Peroxisomal Thiolase.
  • N. Latruffe
  • Biology, Computer Science
    Advances in experimental medicine and biology
  • 2020
TLDR
In the human HepG2 cells, thiolase expression is upregulated by glucose and downregulated by insulin and sterols, while dexamethasone and fatty acids have no effect, and the transcript Tr3 appears to be the most abundant.
Cloning and stress-respondent transcription of 3-ketoacyl-CoA thiolase gene of Isochrysis galbana (Haptophyta)
TLDR
The findings provided an understanding about the response of IgKAT to temperature and nutrition nitrate stresses (those deviating from the normal) at transcription level and will aid the understanding of the gene regulation of β-oxidation pathway in response to culture conditions of I. galbana.
Cocoa protective effects against abnormal fat storage and oxidative stress induced by a high-fat diet involve PPARα signalling activation.
TLDR
When co-administered with the HF diet, cocoa treatment counteracted lipid storage in the liver, improved the lipid-metabolizing activity and oxidative stress defences and normalized the weight gain per calorie consumed.
Treatment with PPARα Agonist Clofibrate Inhibits the Transcription and Activation of SREBPs and Reduces Triglyceride and Cholesterol Levels in Liver of Broiler Chickens
TLDR
The effects of PPARα agonist clofibrate on lipid metabolism in liver of broiler chickens involve inhibiting transcription and activation of SREBPs and SREBP-dependent lipogenic and cholesterologenic gene expression, thereby resulting in a reduction of the triglyceride and cholesterol levels in Liver of Broiler chickens.
Altered liver expression of genes involved in lipid and glucose metabolism in mice with partial IGF-1 deficiency: an experimental approach to metabolic syndrome
TLDR
The mere partial IGF-1 deficiency is responsible for the reduction in the expression of genes involved in glucose and lipid metabolism, resulting in dyslipidemia and hyperglycemia, which may seriously contribute to the establishment of MetS.
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TLDR
It is established that peroxisome proliferation in rodent liver is highly correlatable with the induction mostly of the l- and d-PBE genes, raising the possibility that intermediate metabolites of very long-chain fatty acids andperoxisomal β-oxidation act as ligands for PPARα.
Absence of Spontaneous Peroxisome Proliferation in Enoyl-CoA Hydratase/l-3-Hydroxyacyl-CoA Dehydrogenase-deficient Mouse Liver
TLDR
Results indicate that disruption of classical peroxisomal fatty acid β-oxidation system distal to AOX step does not interfere with the inactivation of endogenous ligands of PPARα, further confirming that the AOX gene is indispensable for the physiological regulation of this receptor.
Human peroxisomal 3-oxoacyl-coenzyme A thiolase deficiency.
  • A. Schram, S. Goldfischer, J. Tager
  • Biology, Computer Science
    Proceedings of the National Academy of Sciences of the United States of America
  • 1987
TLDR
The finding that both very-long-chain fatty acids and abnormal bile acids accumulate in this patient suggests that a single peroxisomal 3-oxoacyl-CoA thiolase is involved in the oxidative chain shortening of bothvery- long-chain acids and the coprostanoic acids.
A role for PPARalpha in the control of SREBP activity and lipid synthesis in the liver.
TLDR
Mice of both genotypes showed the expected decreases in 3-hydroxy-3-methylglutaryl-CoA reductase mRNA levels and cholesterol synthesis in response to an increase in dietary cholesterol, and an accompanying rise in stearoyl-coA desaturase mRNA expression suggested that the increase in lipogenesis could have resulted from an alteration in membrane fatty acid composition that influenced SREBP activation.
Inactivation of the Peroxisomal Multifunctional Protein-2 in Mice Impedes the Degradation of Not Only 2-Methyl-branched Fatty Acids and Bile Acid Intermediates but Also of Very Long Chain Fatty Acids*
TLDR
The present data indicate that MFP-2 is not only essential for the degradation of 2-methyl-branched fatty acids and the bile acid intermediates di- and trihydroxycoprostanic acid but also for the breakdown of very long chain fatty acids.
Probing peroxisomal β-oxidation and the labelling of acetyl-CoA proxies with [1-13C]octanoate and [3-13C]octanoate in the perfused rat liver
TLDR
The goals of the present study were to test whether peroxisomal β-oxidation contributes acetyl groups for malonyl-CoA synthesis, and the degree of labelling homogeneity of acetyl- CoA proxies (acetyl moiety of citrate, acetate, β-hydroxybutyrate, malony l-coA and acetylcarnitine).
Hepatocellular and Hepatic Peroxisomal Alterations in Mice with a Disrupted Peroxisomal Fatty Acyl-coenzyme A Oxidase Gene*
TLDR
Observations demonstrate links among peroxisomal β-oxidation, development of severe microvesicular fatty liver,peroxisome assembly, cell death, and cell proliferation in liver.
Defective peroxisomal catabolism of branched fatty acyl coenzyme A in mice lacking the sterol carrier protein-2/sterol carrier protein-x gene function.
TLDR
Gene targeting in mice supported that the gene disruption led to inefficient import of phytanoyl-CoA into peroxisomes and to defective thiolytic cleavage of 3-ketopristanoysl- CoA.
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