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Hepatic Steatosis and Peroxisomal Fatty Acid Beta-oxidation

[ Vol. 13 , Issue. 10 ]


Mustapha Cherkaoui-Malki, Sailesh Surapureddi, Hammam I. El Hajj, Joseph Vamecq and Pierre Andreoletti   Pages 1412 - 1421 ( 10 )


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.


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


Bio-PeroxIL, EA 7270, Université de Bourgogne, 6 Bd Gabriel Dijon F-21000, France.

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