ArticleBiochemistry2006
Very-long-chain and branched-chain fatty acyl-CoAs are high affinity ligands for the peroxisome proliferator-activated receptor alpha (PPARalpha).
Article in Biochemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
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- Selective autophagy in cancer: mechanisms, therapeutic implications, and future perspectives.Molecular cancer · 2024Review
- Mechanisms Mediating the Regulation of Peroxisomal Fatty Acid Beta-Oxidation by PPARα.International journal of molecular sciences · 2021Review
- Autophagy and organelle homeostasis in cancer.Developmental cell · 2021Review
- Branched-Chain Fatty Acids as Mediators of the Activation of Hepatic Peroxisome Proliferator-Activated Receptor Alpha by a Fungal Lipid Extract.Biomolecules · 2020Article
- Peroxisome Metabolism in Cancer.Cells · 2020Review
- Peroxisome-Deficiency and HIF-2α Signaling Are Negative Regulators of Ketohexokinase Expression.Frontiers in cell and developmental biology · 2020Article
- The PPARPPAR research · 2020Review
- Self-regulation of the inflammatory response by peroxisome proliferator-activated receptors.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Review
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- Sex-dependent impact of Scp-2/Scp-x gene ablation on hepatic phytol metabolism.Archives of biochemistry and biophysics · 2017Article
- Fatty acid binding profile of the liver X receptor α.Journal of lipid research · 2017Article
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- Fenofibrate Decreases Insulin Clearance and Insulin Secretion to Maintain Insulin Sensitivity.The Journal of biological chemistry · 2016Article
- Review
- Impact of SCP-2/SCP-x gene ablation and dietary cholesterol on hepatic lipid accumulation.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Metabolic dysfunctions in multiple sclerosis: implications as to causation, early detection, and treatment, a case control study.BMC neurology · 2015Article
- Structural and functional assessment of perilipin 2 lipid binding domain(s).Biochemistry · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Very-long-chain fatty acids (VLCFA) and branched-chain fatty acids (BCFA) are potent inducers of the peroxisome proliferator-activated receptor PPARalpha, a nuclear receptor that enhances transcription of peroxisomal enzymes mediating beta-oxidation of these potentially toxic fatty acids. However, it is not known whether the respective free fatty acids or their activated metabolites, i.e., CoA thioesters, (i) are the endogenous high-affinity PPARalpha ligands, (ii) alter PPARalpha conformation, and (iii) alter recruitment of coregulatory proteins to PPARalpha. As shown by quenching of PPARalpha intrinsic amino acid fluorescence, PPARalpha exhibited high affinity (3-29 nM Kds) for the CoA thioesters of the common (C20-C24) VLCFA. In contrast, with the exception of arachidonic acid (Kd = 20 nM), PPARalpha only weakly bound the VLCFA. PPARalpha also exhibited higher affinity for the CoA thioesters of BCFA (phytanoyl-CoA, pristanoyl-CoA; Kds near 11 nM) than for the respective free branched-chain fatty acids. As shown by circular dichroism, the high affinity VLCFA-CoA and BCFA-CoA strongly altered PPARalpha conformation. Likewise, the high affinity VLCFA-CoA and BCFA-CoA altered cofactor recruitment to PPARalpha as shown by coimmunoprecipitation from liver homogenates. In contrast, nearly all the respective free fatty acids elicited only weak conformational changes in PPARalpha and did not alter cofactor recruitment to PPARalpha. In summary, the CoA thioesters of very-long-chain and branched-chain fatty acids are much more potent PPARalpha ligands than the free acids, resulting in altered PPARalpha conformation and cofactor recruitment. Since these are hallmarks of ligand-activated nuclear receptors, this suggests that the CoA thioesters are the active forms of these PPARalpha ligands.
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