{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T07:25:58Z","timestamp":1786951558321,"version":"build-2736575974"},"reference-count":40,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T00:00:00Z","timestamp":1784592000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T00:00:00Z","timestamp":1784592000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Autophagy is a key cellular process regulating lipid turnover and maintaining hepatic homeostasis, and its impairment is closely associated with the pathogenesis of nonalcoholic fatty liver disease (NAFLD). In this study, we examined the effects of glucosamine (GlcN), a hexosamine biosynthetic pathway intermediate, on autophagy and lipid accumulation using both human hepatocellular carcinoma (HepG2) cells and a high\u2010fat diet (HFD)\u2010induced NAFLD mouse model. GlcN treatment led to a dose\u2010 and time\u2010dependent increase in the expression of autophagy\u2010related markers LC3 and p62 at both mRNA and protein levels. Pharmacological inhibition of\n                    <jats:italic>O<\/jats:italic>\n                    \u2010GlcNAcase (OGA) further enhanced autophagic activity, whereas inhibition of\n                    <jats:italic>O<\/jats:italic>\n                    \u2010GlcNAc transferase (OGT) abrogated GlcN\u2010induced autophagic responses, implicating\n                    <jats:italic>O<\/jats:italic>\n                    \u2010GlcNAcylation as a key mediator of GlcN\u2010driven autophagy induction. Functionally, GlcN significantly reduced palmitic acid (PA)\u2010induced lipid accumulation in HepG2 cells and alleviated hepatic steatosis in HFD\u2010fed mice, likely through enhancement of autophagic flux. These findings demonstrate that GlcN promotes lipid clearance in hepatocytes via\n                    <jats:italic>O<\/jats:italic>\n                    \u2010GlcNAc\u2010dependent autophagy and highlight its potential as a therapeutic agent for NAFLD and related metabolic disorders.\n                  <\/jats:p>","DOI":"10.1002\/jbt.71042","type":"journal-article","created":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T13:44:24Z","timestamp":1784641464000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Glucosamine Promotes Autophagy and Attenuates Hepatic Steatosis Via\n                    <i>O<\/i>\n                    \u2010GlcNAcylation\u2013Mediated Mechanisms"],"prefix":"10.1002","volume":"40","author":[{"given":"Jiwon","family":"Park","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, College of Medicine Inha University Incheon Korea"},{"name":"Department of Biomedical Science, Program in Biomedical Science and Engineering Inha University Incheon Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong Yeol","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, College of Medicine Inha University Incheon Korea"},{"name":"Department of Biomedical Science, Program in Biomedical Science and Engineering Inha University Incheon Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Quynh T. 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