Nonalcoholic steatosis and steatohepatitis III. Peroxisomal β-oxidation, PPARα, and steatohepatitis

Janardan K Reddy*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

232 Scopus citations


Peroxisomes are involved in the β-oxidation chain shortening of long-chain and very-long-chain fatty acyl-CoAs, long-chain dicarboxylyl-CoAs, the CoA esters of eicosanoids, 2-methyl-branched fatty acyl-CoAs, and the CoA esters of the bile acid intermediates, and in the process, they generate H2O2. There are two complete sets of β-oxidation enzymes present in peroxisomes, with each set consisting of three distinct enzymes. The classic PPARα regulated and inducible set participates in the β-oxidation of straight-chain fatty acids, whereas the second noninducible set acts on branched-chain fatty acids. Long-chain and very long-chain fatty acids are also metabolized by the cytochrome P-450 CYP4A ω-oxidation system to dicarboxylic acids that serve as substrates for peroxisomal β-oxidation. Evidence derived from mouse models of PPARα and peroxisomal β-oxidation deficiency highlights the critical importance of the defects in PPARα-inducible β-oxidation in energy metabolism and in the development of steatohepatitis.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number6 44-6
StatePublished - Dec 1 2001


  • Fatty acid β- and ω-oxidation
  • Peroxisomal biogenesis disorders
  • Peroxisomal pro-liferator-activated receptor α
  • Peroxisomes

ASJC Scopus subject areas

  • Gastroenterology
  • Physiology
  • Physiology (medical)


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