{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T06:59:11Z","timestamp":1790405951252,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T00:00:00Z","timestamp":1789430400000},"content-version":"vor","delay-in-days":14,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"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":["Food Science &amp;amp; Nutrition"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Dyslipidemia, characterized by abnormal levels of serum lipids such as cholesterol and triglycerides, is a significant risk factor for metabolic disorders. Fucoidan, a marine sulfated polysaccharide, has shown anti\u2010inflammatory and lipid\u2010modulating properties, but its mechanism of action in high\u2010fat diet (HFD)\u2010induced dyslipidemia remains unclear. In this study, treatment with fucoidan (50\u2009mg\/kg\/day) did not alter HFD\u2010driven weight gain or food intake, but significantly decreased serum total cholesterol (TC). Although serum high\u2010density lipoprotein cholesterol (HDL\u2010C) was also decreased, this change may reflect normalization of HFD\u2010induced cholesterol homeostasis in mice. Moreover, fucoidan treatment reduced hepatic triglyceride and TC, accompanied by decreasing lipid droplets in the liver, indicating fucoidan is critical for improving HFD\u2010induced hepatic lipid accumulation. RNA\u2010seq analysis revealed that fucoidan reverses HFD\u2010induced downregulation of Defa24, Slc34a1, and Nnt, and may contribute to maintain hepatic metabolic homeostasis. Network pharmacology identified TNF\u03b1 as a candidate key target, and molecular docking suggested a potential interaction between fucoidan and TNF\u03b1. Furthermore, fucoidan suppressed HFD\u2010driven upregulation of TNF\u03b1 and its downstream target Pla2g2f in\u00a0vivo and attenuated TNF\u03b1\u2010induced Pla2g2f expression in RAW264.7 cells. Collectively, these findings suggest that the protective effects of fucoidan against HFD\u2010induced dyslipidemia are associated with regulation of cholesterol metabolism and suppression of TNF\u03b1\u2013Pla2g2f\u2010associated inflammatory signaling, supporting its potential application in dyslipidemia management.<\/jats:p>","DOI":"10.1002\/fsn3.72159","type":"journal-article","created":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T06:01:38Z","timestamp":1789538498000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Therapeutic Effects and Mechanisms of Fucoidan on Dyslipidemia in Obese Mice"],"prefix":"10.1002","volume":"14","author":[{"given":"Lizhi","family":"Peng","sequence":"first","affiliation":[{"name":"Department of Pharmacy, Shenzhen Key Laboratory of Chinese Medicine Active Substance Screening and Translational Research The Seventh Affiliated Hospital of Sun Yat\u2010Sen University  Shenzhen 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