Supplementation of vitamins C and E increases the vitamin E status but does not prevent the formation of oxysterols in the liver of guinea pigs fed an oxidised fat

Keller, U; Brandsch, Corinna; Eder, Klaus

doi:10.1007/s00394-004-0481-3

Cited by 20 publications

(11 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The finding that the body weight development was not affected by the oxidized fat is advantageous from a methodological viewpoint because the effects of the oxidized fat were not confounded by secondary effects of reduced growth. Recent studies have shown that consumption of oxidized fats leads to a reduction of tocopherol concentrations in animal tissues due to a reduced digestibility and an enhanced turnover of vitamin E [8,11,12,43]. The finding of reduced α-tocopherol concentrations in plasma and liver of pigs fed the oxidized fat in the present study indicates that even moderately oxidized fats compromise tissue vitamin E status in animals.…”

Section: Discussionsupporting

confidence: 61%

“…One of the most striking effects of oxidized fat is the induction of oxidative stress which is due to lipid hydroperoxides absorbed from the ingested oxidized fats and reactive oxygen species (ROS) generated from microsomal cytochrome P450 enzymes which are induced by oxidized fat [6-8]. Oxidative stress in animals fed oxidized fats is evident by elevated concentrations of lipid peroxidation products, reduced concentrations of exogenous and endogenous antioxidants, and a decreased ratio of reduced and oxidized glutathione in plasma and tissues [8-13]. …”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Dietary moderately oxidized oil activates the Nrf2 signaling pathway in the liver of pigs

et al. 2012

Self Cite

View full text Add to dashboard Cite

BackgroundPrevious studies have shown that administration of oxidized oils increases gene expression and activities of various enzymes involved in xenobiotic metabolism and stress response in the liver of rats and guinea pigs. As these genes are controlled by nuclear factor erythroid-derived 2-like 2 (Nrf2), we investigated the hypothesis that feeding of oxidized fats causes an activation of that transcription factor in the liver which in turn activates the expression of antioxidant, cytoprotective and detoxifying genes.MethodsTwenty four crossbred pigs were allocated to two groups of 12 pigs each and fed nutritionally adequate diets with either fresh rapeseed oil (fresh fat group) or oxidized rapeseed oil prepared by heating at a temperature of 175°C for 72 h (oxidized fat group).ResultsAfter 29 days of feeding, pigs of the oxidized fat group had a markedly increased nuclear concentration of the transcription factor Nrf2 and a higher activity of cellular superoxide dismutase and T4-UDP glucuronosyltransferase in liver than the fresh fat group (P < 0.05). In addition, transcript levels of antioxidant and phase II genes in liver, like superoxide dismutase 1, heme oxygenase 1, glutathione peroxidase 1, thioredoxin reductase 1, microsomal glutathione-S-transferase 1, UDP glucuronosyltransferase 1A1 and NAD(P)H:quinone oxidoreductase 1 in the liver were higher in the oxidized fat group than in the fresh fat group (P < 0.05). Moreover, pigs of the oxidized fat group had an increased hepatic nuclear concentration of the transcription factor NF-κB which is also an important transcription factor mediating cellular stress response.ConclusionThe present study shows for the first time that administration of an oxidized fat activates the Nrf2 in the liver of pigs which likely reflects an adaptive mechanism to prevent cellular oxidative damage. Activation of the NF-κB pathway might also contribute to this effect of oxidized fat.

show abstract

Section: Discussionsupporting

confidence: 61%

Section: Introductionmentioning

confidence: 99%

Dietary moderately oxidized oil activates the Nrf2 signaling pathway in the liver of pigs

et al. 2012

Self Cite

View full text Add to dashboard Cite

show abstract

“…Although oxidized fat had no effect on proto-oncogene expression in fetal livers in the present study, oxidized fats might be considered critically in view of inducing oxidative stress in different tissues as shown in recent studies [36,37]. In addition, specific components of oxidized fats such as cyclic fatty acid monomers, which are formed in substantial amounts during domestic frying of frozen foods in sunflower oil [38], are probably toxic, e.g.…”

Section: Discussionmentioning

confidence: 58%

Feeding oxidized fat during pregnancy up-regulates expression of PPARα-responsive genes in the liver of rat fetuses

et al. 2007

Self Cite

View full text Add to dashboard Cite

BackgroundFeeding oxidized fats causes activation of peroxisome proliferator-activated receptor α (PPARα) in the liver of rats. However, whether feeding oxidized fat during pregnancy also results in activation of PPARα in fetal liver is unknown. Thus, this study aimed to explore whether feeding oxidized fat during pregnancy causes a PPARα response in fetal liver. Two experiments with pregnant rats which were administered three different diets (control; oxidized fat; clofibrate as positive control) in a controlled feeding regimen during either late pregnancy (first experiment) or whole pregnancy (second experiment) were performed.ResultsIn both experiments pregnant rats treated with oxidized fat or clofibrate had higher relative mRNA concentrations of the PPARα-responsive genes acyl-CoA oxidase (ACO), cytochrome P450 4A1 (CYP4A1), L-type carnitin-palmitoyl transferase I (L-CPT I), medium-chain acyl-CoA dehydrogenase (MCAD), and long-chain acyl-CoA dehydrogenase (LCAD) in the liver than control rats (P < 0.05). In addition, in both experiments fetuses of the oxidized fat group and the clofibrate group also had markedly higher relative mRNA concentrations of ACO, CYP4A1, CPT I, MCAD, and LCAD in the liver than those of the control group (P < 0.05), whereas the relative mRNA concentrations of PPARα, SREBP-1c, and FAS did not differ between treatment groups. In the second experiment treatment with oxidized fat also reduced triacylglycerol concentrations in the livers of pregnant rats and fetuses (P < 0.05).ConclusionThe present study demonstrates for the first time that components of oxidized fat with PPARα activating potential are able to induce a PPARα response in the liver of fetuses. Moreover, the present study shows that feeding oxidized fat during whole pregnancy, but not during late pregnancy, lowers triacylglycerol concentrations in fetal livers.

show abstract

“…A more recent study, moreover, demonstrated that an oxidized fat prepared under deep‐frying conditions causes activation of PPARα in the liver and the vasculature and inhibits atherosclerotic plaque development in the low‐density lipoprotein receptor deficient mouse model of atherosclerosis 76. Although these findings show that oxidized fats exert some beneficial effects, they must not be interpreted in that way that oxidized fats are generally regarded as a health‐promoting component of the diet because oxidized fats were also reported to cause adverse effects 3–6, 8, 10. They rather suggest that oxidized fats are a mixture of chemically distinct substances, some of which exhibit potent regulatory activity on lipid metabolism.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

“…Feeding experiments with rats, guinea pigs, and pigs revealed that ingestion of oxidized fats provokes various effects such as depletion of antioxidants, increase in lipid peroxidation 3–9, impairment of glucose tolerance 10, and alterations of thyroid hormone homeostasis 11–13. In addition, a great number of studies showed that oxidized fats influence lipid metabolism.…”

Section: Introductionmentioning

confidence: 99%

Regulation of genes involved in lipid metabolism by dietary oxidized fat

Ringseis

Eder

2010

Molecular Nutrition Food Res

Self Cite

View full text Add to dashboard Cite

Although oxidized fats are widely considered to have detrimental effects on human health, a large number of feeding studies with experimental animals have consistently demonstrated that oxidized fats, compared with fresh fats, cause a reduction in the concentrations of triacylglycerols and cholesterol in liver and plasma. The reason for these effects became clear when recently it was shown that thermo-oxidized fats contain characteristic substances such as hydroxylated fatty acids and cyclic fatty acid monomers which are potent ligands and activators of peroxisome proliferator-activated receptor α - a transcription factor controlling genes involved in fatty acid and lipoprotein metabolism. In addition, oxidized fats have also been reported to inhibit expression of genes involved in fatty acid synthesis and cholesterol homeostasis. These effects are mediated by inhibiting the maturation of sterol regulatory-element binding proteins, which are transcription factors regulating genes involved in fatty acid synthesis and cholesterol homeostasis. This review summarizes the phenotypical alterations of lipid metabolism observed in feeding studies dealing with oxidized fats and addresses the molecular mechanisms underlying these lipid metabolism alterations, in particular the lipid lowering effects of dietary oxidized fats.

show abstract

Supplementation of vitamins C and E increases the vitamin E status but does not prevent the formation of oxysterols in the liver of guinea pigs fed an oxidised fat

Abstract: The results demonstrated that supplementation of vitamins E and C improves the vitamin E status but does not prevent the formation of lipid oxidation products in the liver of guinea pigs fed oxidised fats.

Cited by 20 publications

References 27 publications

Dietary moderately oxidized oil activates the Nrf2 signaling pathway in the liver of pigs

Dietary moderately oxidized oil activates the Nrf2 signaling pathway in the liver of pigs

Feeding oxidized fat during pregnancy up-regulates expression of PPARα-responsive genes in the liver of rat fetuses

Regulation of genes involved in lipid metabolism by dietary oxidized fat

Contact Info

Product

Resources

About