ArticleLipids in health and disease2007
Feeding oxidized fat during pregnancy up-regulates expression of PPARalpha-responsive genes in the liver of rat fetuses.
Article in Lipids in health and disease, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 36 citations in OpenAlex.
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- Influence of feeding thermally peroxidized soybean oil on growth performance, digestibility, and gut integrity in finishing pigs.Journal of animal science · 2018Article
- Different Effects of Maternal Low-Isoflavone Soy Protein and Genistein Consumption on Hepatic Lipid Metabolism of 21-Day-Old Male Rat Offspring.Nutrients · 2017Article
- EPathology oncology research : POR · 2017Article
- Transplacental induction of fatty acid oxidation in term fetal pigs by the peroxisome proliferator-activated receptor alpha agonist clofibrate.Journal of animal science and biotechnology · 2015Article
- Cubilin expression is monoallelic and epigenetically augmented via PPARs.BMC genomics · 2013Article
- Regulation of Genes Involved in Carnitine Homeostasis by PPARα across Different Species (Rat, Mouse, Pig, Cattle, Chicken, and Human).PPAR research · 2012Article
- Induction of gene pattern changes associated with dysfunctional lipid metabolism induced by dietary fat and exposure to a persistent organic pollutant.Toxicology letters · 2009Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundFeeding oxidized fats causes activation of peroxisome proliferator-activated receptor alpha (PPARalpha) in the liver of rats. However, whether feeding oxidized fat during pregnancy also results in activation of PPARalpha in fetal liver is unknown. Thus, this study aimed to explore whether feeding oxidized fat during pregnancy causes a PPARalpha 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 PPARalpha-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 PPARalpha, 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 PPARalpha activating potential are able to induce a PPARalpha 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.
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