Journal ArticleDOI
Peroxisome proliferating sulphur- and oxy-substituted fatty acid analogues are activated to acyl coenzyme A thioesters.
Asle Aarsland,Rolf K. Berge +1 more
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TLDR
The data suggest that the enzymatic activation of the peroxisome proliferating compounds is essential for their proliferating activity, but the rate of activation does not determine the potency of the proliferators.About:
This article is published in Biochemical Pharmacology.The article was published on 1991-01-01. It has received 70 citations till now. The article focuses on the topics: Acyl-CoA & Tetradecylthioacetic acid.read more
Citations
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Journal ArticleDOI
Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors α and δ
TL;DR: It is shown here that specific FAs, eicosanoids, and hypolipidemic drugs are ligands for PPARα or PPARδ, and a novel conformation-based assay is developed that screens activators for their ability to bind to PPAR α/δ and induce DNA binding.
Journal ArticleDOI
Role of the peroxisome proliferator-activated receptor (PPAR) in mediating the effects of fibrates and fatty acids on gene expression.
TL;DR: It is suggested that PPARs are key messengers responsible for the translation of nutritional and pharmacological stimuli into changes in gene expression and differentiation pathways.
Journal ArticleDOI
The peroxisome proliferator activated receptors (PPARs) and their effects on lipid metabolism and adipocyte differentiation
TL;DR: In rodents, a PPAR alpha-mediated change in the expression of genes involved in fatty acid metabolism lies at the basis of the phenomenon of peroxisome proliferation, a pleiotropic cellular response, mainly limited to liver and kidney and which can lead to hepatocarcinogenesis.
Journal ArticleDOI
Steatohepatitis, spontaneous peroxisome proliferation and liver tumors in mice lacking peroxisomal fatty acyl-coa oxidase:implications for peroxisome proliferator-activated receptor alpha natural ligand metabolism
TL;DR: It is shown that mice deficient in AOX exhibit steatohepatitis, increased hepatic H2O2 levels, and hepatocellular regeneration, leading to a complete reversal of fatty change by 6 to 8 months of age, implicating acyl-CoA and other putative substrates for AOX, as biological ligands for PPARα.
Journal ArticleDOI
Role of Fatty Acid Binding Proteins and Long Chain Fatty Acids in Modulating Nuclear Receptors and Gene Transcription
Friedhelm Schroeder,Anca D. Petrescu,Huan Huang,Barbara P. Atshaves,Avery L. McIntosh,Gregory G. Martin,Heather A. Hostetler,Aude Vespa,Danilo Landrock,Kerstin K. Landrock,H. Ross Payne,Ann B. Kier +11 more
TL;DR: The hypothesis that cytoplasmic lipid binding proteins transfer and channel lipidic ligands into nuclei for initiating nuclear receptor transcriptional activity to provide new lipid nutrient signaling pathways that affect lipid and glucose catabolism and storage is proposed.
References
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Journal ArticleDOI
An electron-transport system associated with the outer membrane of liver mitochondria. A biochemical and morphological study.
TL;DR: Experiments with tritiated NADH are described which demonstrate that this "external" pathway of NADH oxidation resembles stereochemically the NADH-cytochrome c reductase system of liver microsomes, and differs from the respiratory chain-linked NADH dehydrogenase.
Book ChapterDOI
L-Glutamate Dehydrogenases*
Barry R. Goldin,Carl Frieden +1 more
TL;DR: A detailed description of the characteristics of this reaction from a variety of sources is given in this paper, showing that, although all classed as glutamate dehydrogenase, the enzymes are different in terms of kinetic characteristics, metabolic function, and molecular properties.
Journal ArticleDOI
Mitochondrial and peroxisomal fatty acid oxidation in liver homogenates and isolated hepatocytes from control and clofibrate-treated rats.
TL;DR: It was calculated that the contribution of the peroxisomes to fatty acid oxidation was less than 10% both in cells from control and clofibrate-treated animals and remained unchanged in starvation and diabetes.
Journal ArticleDOI
Biochemical mechanisms of induction of hepatic peroxisome proliferation.
TL;DR: The response, in biochemical and morpholog ical terms, of hepatocytes to peroxisome proliferating chemicals is discussed and possible biochemical mechanism(s) whereby these chemicals may produce peroxISome proliferation are focused on.
Related Papers (5)
Induction of peroxisomal β-oxidation in 7800 C1 Morris hepatoma cells in steady state by fatty acids and fatty acid analogues
Øystein Spydevold,Jon Bremer +1 more