{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,19]],"date-time":"2026-03-19T14:24:10Z","timestamp":1773930250043,"version":"3.50.1"},"reference-count":71,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2025,11,23]],"date-time":"2025-11-23T00:00:00Z","timestamp":1763856000000},"content-version":"vor","delay-in-days":22,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,11,1]],"date-time":"2025-11-01T00:00:00Z","timestamp":1761955200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["ift.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Food Science"],"published-print":{"date-parts":[[2025,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:label\/>\n                    <jats:p>\n                      Previous studies have shown that enteromorpha polysaccharide (EP) can improve glucolipid metabolism disorders, but the mechanism remains unclear. In this study, both a high\u2010fat diet\u2010induced NAFLD animal model and a cellular model exposed to free fatty acids (FFAs) were used to explore the intervention effects of EP and its mechanism in glucolipid metabolism disorders. The results revealed that a high\u2010fat diet could induce hepatic steatosis and glucolipid metabolism disorders, along with decreased expression of IRS\u20101 and increased levels of K18, p\u2010K18, p\u2010PI3K, and p\u2010AKT (\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.05). In addition, the serum K18 levels in NAFLD mice were increased. Intervention with EP significantly counteracted the high\u2010fat diet\u2010induced disturbances in glucose and lipid metabolism associated with NAFLD, downregulated the protein expression of hepatic K18, and decreased the levels of p\u2010AKT, p\u2010PI3K\/PI3K, and p\u2010AKT\/AKT (\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.05). Knocking down K18 can directly regulate the PI3K\/AKT signaling pathway. Additionally, the increases in p\u2010PI3K\/PI3K and p\u2010AKT\/AKT induced by FFAs were partially reversed after K18 was knocked down. Consequently, our findings highlight the pivotal regulatory role of K18 in modulating the high\u2010fat diet\u2010induced disturbances in glucolipid metabolism associated with NAFLD. Moreover, EP partially ameliorated glucolipid metabolism disorders via the K18\u2010mediated IRS\u20101\/PI3K\/AKT\/GSK3\u03b2 pathway.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/1750-3841.70713","type":"journal-article","created":{"date-parts":[[2025,11,24]],"date-time":"2025-11-24T04:36:38Z","timestamp":1763958998000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Enteromorpha Polysaccharides Alleviate High\u2010Fat Diet\u2010Induced Glucolipid Metabolism Disorders via the K18\u2010Mediated IRS\u20101\/PI3K\/AKT\/GSK3\u03b2 Pathway"],"prefix":"10.1111","volume":"90","author":[{"given":"Bingbing","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Health Inspection and Quarantine, School of Public Health Fujian Medical University  Fuzhou Fujian 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