title: Hepatic steatosis and peroxisomal fatty acid beta-oxidation.
abstract: Three subhepatocellular compartments concur for fatty acids degradation including ω-oxidation in endoplasmic reticulum and β-oxidation in both mitochondria and peroxisomes. Deficits affecting the peroxisomal physiology may be associated with multiple metabolic disturbances. Nowadays, a growing body of evidence underlines the key role of peroxisomal β-oxidation in the sensing of lipid metabolism through the production/degradation of some essential metabolites. Lessons from several mice models strengthen the link between fatty acid β-oxidation in peroxisomes and the nuclear hormone receptor Peroxisome Proliferator-Activated Receptor (PPAR)-α with an additional level of coregualtor complexity, which couples regulation of body energetic balance and hepatic caloric flux to functional peroxisome status. Here, we review key determinants of disrupted peroxisomal β-oxidation pathway, which in liver promotes hepatic steatosis and hepatocarcinogenesis.
authors.affiliation: Laboratoire de Biochimie du Peroxysome, Inflammation et Métabolisme Lipidique (Bio-PeroxIL, EA 7270), Université de Bourgogne, Dijon F-21000, France. malki@u-bourgogne.fr
authors.forename: Mustapha
authors.initials: M
authors.lastname: Cherkaoui-Malki
authors.forename: Sailesh
authors.initials: S
authors.lastname: Surapureddi
authors.forename: Hammam I
authors.initials: HI
authors.lastname: El-Hajj
authors.forename: Joseph
authors.initials: J
authors.lastname: Vamecq
authors.forename: Pierre
authors.initials: P
authors.lastname: Andreoletti
mesh_terms: D000818:Animals; D005227:Fatty Acids / Q000378:metabolism*; D005234:Fatty Liver / Q000378:metabolism*; D006801:Humans; D008113:Liver Neoplasms / Q000378:metabolism; D010084:Oxidation-Reduction; D047493:PPAR alpha / Q000378:metabolism; D020675:Peroxisomes / Q000378:metabolism*
chemical_list: D005227:Fatty Acids; D047493:PPAR alpha