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The pathogenesis of MASLD alters the secretion of hepatokines such as fibrinogen\u2010like 1 (FGL1), a candidate mediator of liver steatosis and hyperglycemia. To investigate the contribution of FGL1 to liver diseases, we compared wild\u2010type mice to mice with hepatocyte\u2010specific deletion of\n                    <jats:italic>Fgl1<\/jats:italic>\n                    subjected to a steatosis or HCC experimental protocol. We found that mice deficient for\n                    <jats:italic>Fgl1<\/jats:italic>\n                    in hepatocytes showed higher levels of plasma glucose, pronounced metabolic alterations, and liver injury when fed a western diet compared to their wild\u2010type counterparts. However, both genotypes exhibited similar lipid deposition in the liver. Similarly, wild type and\n                    <jats:italic>Fgl1<\/jats:italic>\n                    \u2010deficient mice displayed comparable liver alterations during HCC progression. We observed that\n                    <jats:italic>FGL1<\/jats:italic>\n                    expression was repressed during MASLD progression in mice and humans concomitantly with the severity of liver injury. Altogether, these findings suggest that FGL1 is not a major contributor to the pathogenesis of MASLD and HCC.\n                  <\/jats:p>","DOI":"10.1096\/fj.202501997r","type":"journal-article","created":{"date-parts":[[2025,8,20]],"date-time":"2025-08-20T09:42:26Z","timestamp":1755682946000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Ablation of Hepatocyte Derived\u2010\n                    <scp>FGL1<\/scp>\n                    Does Not Aggravate Metabolic Dysfunction\u2010Associated Steatotic Liver Disease"],"prefix":"10.1096","volume":"39","author":[{"given":"Jean","family":"Personnaz","sequence":"first","affiliation":[{"name":"IRSD, INSERM, INRAE, ENVT, Univ Toulouse III\u2014Paul Sabatier (UPS) Universit\u00e9 de Toulouse  Toulouse France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa","family":"Cannizzo","sequence":"additional","affiliation":[{"name":"IRSD, INSERM, INRAE, ENVT, 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