ArticleThe Journal of nutritional biochemistry2017
PPARα protects against trans-fatty-acid-containing diet-induced steatohepatitis.
Article in The Journal of nutritional biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Elaidic acid drives cellular senescence and inflammation via lipid raft-mediated IL-1R signaling.iScience · 2025Article
- Perfluorooctane sulfonate exposure and alcohol-associated liver disease severity in a mouse chronic-binge ethanol feeding model.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Associations between trans fatty acids and systemic immune-inflammation index: a cross-sectional study.Lipids in health and disease · 2024Article
- Long noncoding RNAJournal of biomedical research · 2023Article
- Article
- Molecular mechanisms of metabolic associated fatty liver disease (MAFLD): functional analysis of lipid metabolism pathways.Clinical science (London, England : 1979) · 2022Review
- Acidic Activated Charcoal Prevents Obesity and Insulin Resistance in High-Fat Diet-Fed Mice.Frontiers in nutrition · 2022Article
- Impact of Dietary Fat on the Progression of Liver Fibrosis: Lessons from Animal and Cell Studies.International journal of molecular sciences · 2021Review
- Trans Fatty Acid Intake Induces Intestinal Inflammation and Impaired Glucose Tolerance.Frontiers in immunology · 2021Article
- A saturated fatty acid-rich diet enhances hepatic lipogenesis and tumorigenesis in HCV core gene transgenic mice.The Journal of nutritional biochemistry · 2020Article
- Dietary Restriction Suppresses Steatosis-Associated Hepatic Tumorigenesis in Hepatitis C Virus Core Gene Transgenic Mice.Liver cancer · 2020Article
- Review
- Mechanisms of Action of trans Fatty Acids.Advances in nutrition (Bethesda, Md.) · 2020Review
- A trans-fatty acid-rich diet promotes liver tumorigenesis in HCV core gene transgenic mice.Carcinogenesis · 2020Article
- PPARs as Metabolic Regulators in the Liver: Lessons from Liver-Specific PPAR-Null Mice.International journal of molecular sciences · 2020Review
- High-trans fatty acid and high-sugar diets can cause mice with non-alcoholic steatohepatitis with liver fibrosis and potential pathogenesis.Nutrition & metabolism · 2020Article
- Industrial Trans Fatty Acids Stimulate SREBP2-Mediated Cholesterogenesis and Promote Non-Alcoholic Fatty Liver Disease.Molecular nutrition & food research · 2019Article
- Peroxisome proliferator-activated receptor α attenuates high-cholesterol diet-induced toxicity and pro-thrombotic effects in mice.Archives of toxicology · 2019Article
- Chronic consumption of fructose in combination with trans fatty acids but not with saturated fatty acids induces nonalcoholic steatohepatitis with fibrosis in rats.European journal of nutrition · 2018Article
- Targeting nuclear receptors for the treatment of fatty liver disease.Pharmacology & therapeutics · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Consumption of trans-fatty acids (TFA), unsaturated fatty acids (FA) containing trans double bonds, is a risk factor for metabolic syndrome and steatohepatitis. Peroxisome proliferator-activated receptor α (PPARα) is a master regulator of hepatic lipid homeostasis. To examine the contribution of PPARα to changes in liver phenotypes induced by TFA, two diets were used: a purified control diet and an isocaloric diet in which most of the soybean oil, a major source of FA in the diet, was replaced with TFA-rich shortening. The diets were fed to wild-type and Ppara-null mice for 2 months. Ppara-null mice fed a TFA-containing diet showed more severe hepatic steatosis and liver damage compared with similarly treated wild-type mice, as revealed by increased hepatic triglyceride (TG) contents and serum alanine aminotransferase activities. While the TFA-rich diet increased the hepatic expression of enzymes involved in de novo FA synthesis and decreased TG-hydrolyzing enzymes in both genotypes, the expression of FA-catabolizing enzymes was decreased in Ppara-null mice, resulting in more severe hepatosteatosis. Additionally, the expression levels of key contributors to inflammation, such as osteopontin, were increased, and nuclear factor-kappa B was activated in TFA-containing diet-fed Ppara-null mice. Enhanced inflammatory signaling in these mice was presumably mediated by toll-like receptor 2, with no accompanying inflammasome activation. Collectively, these results suggest a protective role for PPARα in the pathological changes in the liver following TFA consumption. PPARα might prevent TFA-containing diet-induced steatohepatitis.
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