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Journal of Lipid Research, Vol. 43, 557-564, April 2002
Copyright © 2002 by Lipid Research, Inc.

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

Correspondence to: Sampath Parthasarathy, To whom correspondence should be addressed., spartha{at}emory.edu (E-mail)

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- (PPAR-). mRNA and PPAR- ligand could increase apoA-I secretion in these cells.

Therefore we propose that the mechanism for the induction of apoA-I might include PPAR- for which oxidized fatty acid is a ligand.—Rong, R., S. Ramachandran, M. Penumetcha, N. Khan, and S. Parthasarathy. Dietary oxidized fatty acids may enhance intestinal apolipoprotein A-I production. J. Lipid Res. 2002. 43: 557–564.

Supplementary key words: atherosclerosis, oxidized linoleic acid, Caco-2 cells, high density lipoprotein, oxidative stress, brush border, 13-HPODE, 13-HODE, antioxidant defense, oxidized low density lipoprotein, apolipoprotein B, PPAR-

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