{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:02:27Z","timestamp":1792022547589,"version":"4.4.0"},"reference-count":46,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2025,4,15]],"date-time":"2025-04-15T00:00:00Z","timestamp":1744675200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82400933"],"award-info":[{"award-number":["82400933"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["dom-pubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2025,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>Abnormal lipid accumulation is an important cause of metabolic dysfunction\u2010associated fatty liver disease (MAFLD) progression and can induce several stress responses within cells. This study is the first to explore the role and molecular mechanism of stress granules (SGs) in MAFLD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A gene knock\u2010down model of G3BP1, a core SG molecule in mice and HepG2 cells, was constructed to explore the role of SGs in MAFLD induced in vivo by a high\u2010fat diet or in vitro by palmitic acid (PA). Methods included metabolic phenotyping; western blotting; qPCR; and immunofluorescence, haematoxylin\/eosin and masson staining. The downstream molecules of G3BP1 and its specific molecular mechanism were screened using RNA sequencing (RNA\u2010seq).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>G3BP1 and TIA1 expression were upregulated in high\u2010fat diet\u2010fed mouse liver tissues and PA\u2010induced HepG2 cells, and the two molecules showed significantly increased colocalisation. G3BP1 knock\u2010down slightly increased TIA1 expression in the livers of obese mice but not in lean mice. G3BP1 deficiency aggravated liver lipid deposition and insulin resistance in obese mice, and this phenotype was confirmed in vitro in PA\u2010induced hepatocytes. RNA\u2010seq demonstrated that G3BP1 slowed down MAFLD progression by inhibiting APOC3, possibly through a mechanistic suppression of APOC3 entry into the nucleus.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study reveals for the first time a protective role for SGs in MAFLD. Specifically, knocking down the core G3BP1 molecule in SGs aggravated the progression of fatty acid\u2010induced MAFLD through a mechanism that may involve the nuclear entry of APOC3. These findings provide a new therapeutic direction for MAFLD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.16302","type":"journal-article","created":{"date-parts":[[2025,4,15]],"date-time":"2025-04-15T03:21:51Z","timestamp":1744687311000},"page":"2985-2995","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["<scp>G3BP1<\/scp>\n                    , a stress granule core protein, ameliorates metabolic dysfunction\u2010associated fatty liver disease by attenuating hepatocyte lipid deposition"],"prefix":"10.1111","volume":"27","author":[{"given":"Xingjing","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Endocrinology The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University  China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huimei","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Endocrinology Huai'an Hospital 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