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
Current Drug Metabolism
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.
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Cite this article as:
Cherkaoui-Malki Mustapha, Surapureddi Sailesh, I. El Hajj Hammam, Vamecq Joseph and Andreoletti Pierre, Hepatic Steatosis and Peroxisomal Fatty Acid Beta-oxidation, Current Drug Metabolism 2012; 13 (10) . https://dx.doi.org/10.2174/138920012803762765
DOI https://dx.doi.org/10.2174/138920012803762765 |
Print ISSN 1389-2002 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5453 |
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