Oxidized fat induces oxidative stress but has no effect on NF-kappaB-mediated proinflammatory gene transcription in porcine intestinal epithelial cells

Inflamm Res. 2007 Mar;56(3):118-25. doi: 10.1007/s00011-006-6122-y.


Objective and design: The effect of oxidized frying oils on PPARgamma which is a potent inhibitor of inflammatory responses in the intestine is currently unknown. Thus, the present study aimed to explore the effect of oxidized frying oil on PPARgamma DNA-binding and proinflammatory responses in intestinal epithelial cells.

Material and methods: 18 male pigs were fed two different diets containing either fresh fat or oxidized fat (n = 9 each). After 28 d, intestinal epithelial cells were isolated and analyzed for PPARgamma DNA-binding, NF-kappaB DNA-binding and NF-kappaB target gene expression. In addition, markers of lipid peroxidation and antioxidant status were determined.

Results: Feeding the oxidized fat slightly, but not significantly, activated PPARgamma DNA-binding in intestinal epithelial cells when compared to fresh fat. In addition, oxidized fat increased the concentration of TBARS and reduced the concentrations of alpha-tocopherol and activities of antioxidant enzymes relative to fresh fat (P < 0.05). No effect of the oxidized fat was observed on NF-kappaB DNA-binding and NF-kappaB target gene expression in intestinal epithelial cells.

Conclusions: The present study suggests that moderate PPARgamma activation and induction of oxidative stress by oxidized frying oil have no implication for NF-kappaB-mediated proinflammatory gene expression in porcine intestinal epithelial cells.

MeSH terms

  • Animal Feed
  • Animals
  • Antioxidants / metabolism
  • Apolipoprotein A-I / blood
  • Body Weight / drug effects
  • Catalepsy / genetics
  • Catalepsy / metabolism
  • Cholesterol, HDL / blood
  • DNA / metabolism
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism*
  • Fats / metabolism
  • Fats / pharmacology*
  • Gene Expression Regulation
  • Inflammation Mediators / metabolism*
  • Intestinal Mucosa / metabolism*
  • Intestines / drug effects*
  • Male
  • NF-kappa B / metabolism*
  • Oxidation-Reduction
  • Oxidative Stress / drug effects
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Protein Binding
  • RNA, Messenger / genetics
  • Thiobarbituric Acid Reactive Substances / metabolism
  • Transcription, Genetic / genetics


  • Antioxidants
  • Apolipoprotein A-I
  • Cholesterol, HDL
  • Fats
  • Inflammation Mediators
  • NF-kappa B
  • PPAR gamma
  • RNA, Messenger
  • Thiobarbituric Acid Reactive Substances
  • DNA