Title:Hepatic Steatosis and Peroxisomal Fatty Acid Beta-oxidation
Volume: 13
Issue: 10
Author(s): Mustapha Cherkaoui-Malki, Sailesh Surapureddi, Hammam I. El Hajj, Joseph Vamecq and Pierre Andreoletti
Affiliation:
Keywords:
ACOX1, Coactivators, hepatic Steatosis, hepatocarcinogenesis, MED1, NASH, beta-oxidation, Peroxisome, Peroxisomes proliferation,
PPARalpha
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.
