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Updated: May 18, 2026

Measurement of Fatty Acid β-Oxidation in a Suspension of Freshly Isolated Mouse Hepatocytes
Published on: September 9, 2021
Hepatic steatosis and peroxisomal fatty acid beta-oxidation
Mustapha Cherkaoui-Malki1, Sailesh Surapureddi, Hammam I El-Hajj
1Laboratoire de Biochimie du Peroxysome, Inflammation et Métabolisme Lipidique (Bio-PeroxIL, EA 7270), Université de Bourgogne, Dijon F-21000, France. malki@u-bourgogne.fr
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.
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