Dietary oxidized fatty acids may enhance intestinal apolipoprotein A-I production

Rong Rong, Sumathi Ramachandran, Meera Penumetcha, Nadya Khan, Sampath Parthasarathy*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)


Apolipoprotein (apo)A-I, the major protein component of HDL, is synthesized principally in the small intestine and liver. Recently we observed an increase in plasma apoA-I level in humans who were on an oxidized fat diet. To test whether oxidized fatty acids could affect apoA-I synthesis, we incubated day 4 (undifferentiated) and day 14 (differentiated) Caco-2 cells with varying concentrations of oxidized linoleic acid (ox-linoleic acid) (5, 10, and 25 μM) and unoxidized linoleic acid for 24 h. Ox-linoleic acid caused a dose-dependent increase in the levels of apoA-I protein in both differentiated and undifferentiated Caco-2 cells as assessed by ELISA and Western blot analysis. Whereas apoB production was not increased by ox-linoleic acid in both day 4 and day 14 Caco-2 cells. The mRNA expression for apoA-I paralleled the protein expression when measured by RT-PCR. We also found that both day 4 and day 14 Caco-2 cells did express peroxisomal proliferator-activated receptor-γ (PPAR-γ). mRNA and PPAR-γ ligand could increase apoA-I secretion in these cells. Therefore we propose that the mechanism for the induction of apoA-I might include PPAR-γ for which oxidized fatty acid is a ligand.

Original languageEnglish
Pages (from-to)557-564
Number of pages8
JournalJournal of Lipid Research
Issue number4
Publication statusPublished - 2002
Externally publishedYes


  • 13-HODE
  • 13-HPODE
  • Antioxidant defense
  • Apolipoprotein B
  • Atherosclerosis
  • Brush border
  • Caco-2 cells
  • High density lipoprotein
  • Oxidative stress
  • Oxidized linoleic acid
  • Oxidized low density lipoprotein
  • PPAR-γ

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