ArticleScientific reports2020
The food contaminant deoxynivalenol provokes metabolic impairments resulting in non-alcoholic fatty liver (NAFL) in mice.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Recent advances in the mechanism of deoxynivalenol-induced hepatotoxicity and protective strategies.Archives of toxicology · 2026Review
- Zearalenone exposure may increase the risk of non-alcoholic fatty liver disease by activating CYP1B1-SCD1.Current research in toxicology · 2026Article
- The role of mycotoxins in lipid metabolism and homeostasis: a systematic review.Frontiers in toxicology · 2026Review
- Metabolic disruption by mycotoxins: focus on metabolic endpoints steatosis, adipogenesis and glucose metabolism in vivo and in vitro.Archives of toxicology · 2025Review
- Necroptosis contributes to deoxynivalenol-induced liver injury and inflammation in weaned piglets.Journal of animal science and biotechnology · 2024Article
- 3,5-Dimethyl-2,4,6-trimethoxychalcone Lessens Obesity and MAFLD in Leptin-DeficientInternational journal of molecular sciences · 2024Article
- Effects of Deoxynivalenol and Its Acetylated Derivatives on Lipid Metabolism in Human Normal Hepatocytes.Toxins · 2024Article
- Article
- Constitutively active microglial populations limit anorexia induced by the food contaminant deoxynivalenol.Journal of neuroinflammation · 2022Article
- Deoxynivalenol induces caspase-3/GSDME-dependent pyroptosis and inflammation in mouse liver and HepaRG cells.Archives of toxicology · 2022Article
- Orphan Nuclear Receptor RORγ Modulates the Genome-Wide Binding of the Cholesterol Metabolic Genes during Mycotoxin-Induced Liver Injury.Nutrients · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ribotoxin deoxynivalenol (DON) is a trichothecene found on cereals responsible for mycotoxicosis in both humans and farm animals. DON toxicity is characterized by reduced food intake, diminished nutritional efficiency and immunologic effects. The present study was designed to further characterize the alterations in energy metabolism induced by DON intoxication. We demonstrated that acute DON intoxication triggered liver steatosis associated with an altered expression of genes related to lipids oxidation, lipogenesis and lipolysis. This steatosis was concomitant to anorexia, hypoglycemia and a paradoxical transient insulin release. DON treatment resulted also in stimulation of central autonomic network regulating sympathetic outflow and adrenaline and glucocorticoids secretion. Furthermore, an increased expression of genes linked to inflammation and reticulum endoplasmic stress was observed in the liver of DON-treated mice. Finally, we propose that lipids mobilization from adipose tissues (AT) induced by DON intoxication drives hepatic steatosis since (1) genes encoding lipolytic enzymes were up-regulated in AT and (2) plasma concentration of triglycerides (TGs) and non-esterified fatty acids were increased during DON intoxication. Altogether, these data demonstrate that DON induced hormonal and metabolic dysregulations associated with a spectrum of hepatic abnormalities, evocative of a non-alcoholic fatty liver disease.
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