{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T17:17:29Z","timestamp":1792603049991,"version":"4.5.0"},"reference-count":31,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2024,5,27]],"date-time":"2024-05-27T00:00:00Z","timestamp":1716768000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Drug Development Research"],"published-print":{"date-parts":[[2024,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Asprosin (ASP) is a newly\u2010identified adipokine and plays important roles in energy metabolism homeostasis. However, there is no report on whether and how ASP is involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Therefore, in the study, we investigated the protective effects of ASP\u2010deficiency on the liver in the NAFLD model mice and the detrimental effects of ASP treatment on the human normal hepatocytes (LO2 cell line). More important, we explored the underlying mechanism from the perspective of lipid metabolism and inflammation. In the in vivo experiments, our data showed that the ASP\u2010deficiency significantly alleviated the high\u2010fat diet\u2010induced inflammation and NAFLD, inhibited the hepatic fat deposition and downregulated the expressions of fat acid synthase (FASN), peroxisome proliferator\u2010activated receptor \u03b3 (PPAR\u03b3) and forkhead box protein O1 (FOXO1); moreover, the ASP\u2010deficiency attenuated the inflammatory state and inhibited the activation of the IKK\/NF\u2010\u03baBp65 inflammation pathway. In the in vitro experiments, our results revealed that ASP treatment caused and even exacerbated the injury of LO2 cells induced by FFA; In contrast, the ASP treatment upregulated the expressions of PPAR\u03b3, FOXO1, FASN, ACC and acyl\u2010CoA oxidase 1 (ACOX1) and elevated the reactive oxygen species (ROS) levels. Accordingly, these results demonstrate that ASP causes NAFLD through disrupting lipid metabolism and promoting the inflammation mediated by ROS.<\/jats:p>","DOI":"10.1002\/ddr.22213","type":"journal-article","created":{"date-parts":[[2024,5,27]],"date-time":"2024-05-27T03:34:06Z","timestamp":1716780846000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Asprosin aggravates nonalcoholic fatty liver disease via inflammation and lipid metabolic disturbance mediated by reactive oxygen species"],"prefix":"10.1002","volume":"85","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-9399-6511","authenticated-orcid":false,"given":"Chaowen","family":"Wang","sequence":"first","affiliation":[{"name":"Provincial Key Laboratory of Basic Pharmacology Nanchang University Nanchang China"},{"name":"Department of Pharmacology, School of Pharmacy Nanchang University Nanchang 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