β-Oxidation in hepatocyte cultures from mice with peroxisomal gene knockouts

Ruud Dirkx, Els Meyhi, Stanny Asselberghs, Janardan Reddy, Myriam Baes*, Paul P. Van Veldhoven

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

β-Oxidation of carboxylates takes place both in mitochondria and peroxisomes and in each pathway parallel enzymes exist for each conversion step. In order to better define the substrate specificities of these enzymes and in particular the elusive role of peroxisomal MFP-1, hepatocyte cultures from mice with peroxisomal gene knockouts were used to assess the consequences on substrate degradation. Hepatocytes from mice with liver selective elimination of peroxisomes displayed severely impaired oxidation of 2-methylhexadecanoic acid, the bile acid intermediate trihydroxycholestanoic acid (THCA), and tetradecanedioic acid. In contrast, mitochondrial β-oxidation rates of palmitate were doubled, despite the severely affected inner mitochondrial membrane. As expected, β-oxidation of the branched chain compounds 2-methylhexadecanoic acid and THCA was reduced in hepatocytes from mice with inactivation of MFP-2. More surprisingly, dicarboxylic fatty acid oxidation was impaired in MFP-1 but not in MFP-2 knockout hepatocytes, indicating that MFP-1 might play more than an obsolete role in peroxisomal β-oxidation.

Original languageEnglish (US)
Pages (from-to)718-723
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume357
Issue number3
DOIs
StatePublished - Jun 8 2007

Keywords

  • Branched chain fatty acid
  • Dicarboxylic fatty acid
  • Hepatocyte culture
  • Mitochondria
  • Peroxisome
  • THCA
  • β-Oxidation

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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