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As some mycotoxins act as endocrine disruptors, their structural similarity may lead to effects in lipid and glucose metabolism as well. Via systematic literature search, we mapped the potential of mycotoxins to cause metabolic disruption. Our systematic data search involved mycotoxin keywords combined with metabolic disruption keywords. The retrieved 31 studies revealed 24 in vivo studies, and 18 in vitro studies in total of 13 different mycotoxins. Most studied parameters were triglycerides from blood or liver, followed by total cholesterol and glucose or insulin levels. In vitro studies most often aimed to reveal mechanisms of metabolic disruption, but common metabolic parameters (lipid or cholesterol accumulation). In general, mycotoxin exposure showed a trend towards positive metabolic effects, such as reduction of blood triglycerides levels. Emodin was the most studied mycotoxin. Other mycotoxins were studied in one to three studies. Positive effects were also identified for equisetin, fumonisin B1, fumigaclavine C and ergostatrien-3-B-ol. Adverse effects (e.g. increased lipid deposition to liver) were identified for aflatoxin B1, ochratoxin A, deoxynivalenol, citreoviridin, T-2 toxin and paxilline. As demonstrated by the evaluated in vivo and in vitro studies, mycotoxins seem to have more positive than negative effects on metabolism. However, based on the available data, a general conclusion on the role of mycotoxins as a group cannot be made.<\/jats:p>","DOI":"10.1007\/s00204-025-03957-w","type":"journal-article","created":{"date-parts":[[2025,2,9]],"date-time":"2025-02-09T02:29:11Z","timestamp":1739068151000},"page":"1749-1767","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Metabolic disruption by mycotoxins: focus on metabolic endpoints steatosis, adipogenesis and glucose metabolism in vivo and in vitro"],"prefix":"10.1007","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-9268-0406","authenticated-orcid":false,"given":"Tia","family":"Heikkinen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6439-4403","authenticated-orcid":false,"given":"Jenni","family":"K\u00fcblbeck","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2205-6323","authenticated-orcid":false,"given":"Jaana","family":"Rys\u00e4","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,2,9]]},"reference":[{"key":"3957_CR1","doi-asserted-by":"publisher","DOI":"10.1038\/nm.3159","author":"M Ahmadian","year":"2013","unstructured":"Ahmadian M, Suh JM, Hah N et al (2013) PPAR\u03b3 signaling and metabolism: the good, the bad and the future. 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