ArticleToxicological sciences : an official journal of the Society of Toxicology2014
Role of cholecystokinin in anorexia induction following oral exposure to the 8-ketotrichothecenes deoxynivalenol, 15-acetyldeoxynivalenol, 3-acetyldeoxynivalenol, fusarenon X, and nivalenol.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 44 citations in OpenAlex.
- Mycotoxin contamination in food and feed: Occurrence, co-occurrence, combined impacts on human and animal health, climate change implications, risk assessment, and mitigation strategies.Mycotoxin research · 2026Review
- Comprehensive insights into emerging advances in the Neurobiology of anorexia.Journal of advanced research · 2026Review
- Regulation of PVT-CeA Circuit in Deoxynivalenol-Induced Anorexia and Aversive-Like Emotions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Proinflammatory cytokines interleukin-18 and interleukin-6 mediate anorexia induction by trichothecene deoxynivalenol and its congeners.Frontiers in veterinary science · 2024Article
- A Novel CCK Receptor GPR173 Mediates Potentiation of GABAergic Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Deoxynivalenol (Vomitoxin)-Induced Anorexia Is Induced by the Release of Intestinal Hormones in Mice.Toxins · 2021Article
- Type A Trichothecene Diacetoxyscirpenol-Induced Emesis Corresponds to Secretion of Peptide YY and Serotonin in Mink.Toxins · 2020Article
- Hydrogen-Rich Water and Lactulose Protect Against Growth Suppression and Oxidative Stress in Female Piglets FedToxins · 2018Article
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- Nitric oxide mediates apoptosis and mitochondrial dysfunction and plays a role in growth hormone deficiency by nivalenol in GH3 cells.Scientific reports · 2017Article
- Risks to human and animal health related to the presence of deoxynivalenol and its acetylated and modified forms in food and feed.EFSA journal. European Food Safety Authority · 2017Article
- Appropriateness to set a group health based guidance value for nivalenol and its modified forms.EFSA journal. European Food Safety Authority · 2017Article
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- A novel Peptide-binding motifs inference approach to understand deoxynivalenol molecular toxicity.Toxins · 2015Review
- Deoxynivalenol (Vomitoxin)-Induced Cholecystokinin and Glucagon-Like Peptide-1 Release in the STC-1 Enteroendocrine Cell Model Is Mediated by Calcium-Sensing Receptor and Transient Receptor Potential Ankyrin-1 Channel.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Comparison of anorectic and emetic potencies of deoxynivalenol (vomitoxin) to the plant metabolite deoxynivalenol-3-glucoside and synthetic deoxynivalenol derivatives EN139528 and EN139544.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Comparison of Anorectic Potencies of the Trichothecenes T-2 Toxin, HT-2 Toxin and Satratoxin G to the Ipecac Alkaloid Emetine.Toxicology reportsArticle
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Cereal grain contamination by trichothecene mycotoxins is known to negatively impact human and animal health with adverse effects on food intake and growth being of particular concern. The head blight fungus Fusarium graminearum elaborates five closely related 8-ketotrichothecene congeners: (1) deoxynivalenol (DON), (2) 3-acetyldeoxynivalenol (3-ADON), (3) 15-acetyldeoxynivalenol (15-ADON), (4) fusarenon X (FX), and (5) nivalenol (NIV). While anorexia induction in mice exposed intraperitoneally to DON has been linked to plasma elevation of the satiety hormones cholecystokinin (CCK) and peptide YY₃₋₃₆ (PYY₃₋₃₆), the effects of oral gavage of DON or of other 8-keotrichothecenes on release of these gut peptides have not been established. The purpose of this study was to (1) compare the anorectic responses to the aforementioned 8-ketotrichothecenes following oral gavage at a common dose (2.5 mg/kg bw) and (2) relate these effects to changes plasma CCK and PYY₃₋₃₆ concentrations. Elevation of plasma CCK markedly corresponded to anorexia induction by DON and all other 8-ketotrichothecenes tested. Furthermore, the CCK1 receptor antagonist SR 27897 and the CCK2 receptor antagonist L-365,260 dose-dependently attenuated both CCK- and DON-induced anorexia, which was consistent with this gut satiety hormone being an important mediator of 8-ketotrichothecene-induced food refusal. In contrast to CCK, PYY₃₋₃₆ was moderately elevated by oral gavage with DON and NIV but not by 3-ADON, 15-ADON, or FX. Taken together, the results suggest that CCK plays a major role in anorexia induction following oral exposure to 8-ketotrichothecenes, whereas PYY₃₋₃₆ might play a lesser, congener-dependent role in this response.
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