Hepatic Steatosis and Peroxisomal Fatty Acid Beta-oxidation

Author(s): Mustapha Cherkaoui-Malki , Sailesh Surapureddi , Hammam I. El Hajj , Joseph Vamecq , Pierre Andreoletti .

Journal Name: Current Drug Metabolism

Volume 13 , Issue 10 , 2012


Abstract:

Three subhepatocellular compartments concur for fatty acids degradation including β-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.

Keywords: ACOX1, Coactivators, hepatic Steatosis, hepatocarcinogenesis, MED1, NASH, beta-oxidation, Peroxisome, Peroxisomes proliferation, PPARalpha

Rights & PermissionsPrintExport Cite as


Article Details

VOLUME: 13
ISSUE: 10
Year: 2012
Page: [1412 - 1421]
Pages: 10
DOI: 10.2174/138920012803762765
Price: $58

Article Metrics

PDF: 42