6533b839fe1ef96bd12a6577
RESEARCH PRODUCT
Hepatic steatosis and peroxisomal fatty acid beta-oxidation.
Sailesh SurapureddiMustapha Cherkaoui-malkiJoseph VamecqHammam I El-hajjPierre Andreolettisubject
Pharmacologychemistry.chemical_classificationClinical BiochemistryFatty AcidsLiver NeoplasmsFatty acidPeroxisome proliferator-activated receptorLipid metabolismPeroxisomeBiologyFatty acid beta-oxidationmedicine.diseaseFatty LiverchemistryBiochemistrymedicinePeroxisomesAnimalsHumansPPAR alphaPeroxisome proliferator-activated receptor alphaSteatosisFlux (metabolism)Oxidation-Reductiondescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2012-10-01 | Current drug metabolism |