biostudies-literaturePersonnaz JFondation ARC pour la Recherche sur le CancerAgence Nationale de la Recherche (ANR)Agence Nationale de la RechercheEuropean Research CouncilFondation pour la Recherche Médicale (FRM)Fondation pour la Recherche MédicaleFondation ARC pour la Recherche sur le Cancer (ARC)e70962https://www.ebi.ac.uk/biostudies/studies/S-EPMC12365863biostudies-literatureUnknown39(16)Metabolic dysfunction-associated steatotic liver disease (MASLD) begins with simple steatosis, which can progress to hepatocellular carcinoma (HCC). The pathogenesis of MASLD alters the secretion of hepatokines such as fibrinogen-like 1 (FGL1), a candidate mediator of liver steatosis and hyperglycemia. To investigate the contribution of FGL1 to liver diseases, we compared wild-type mice to mice with hepatocyte-specific deletion of Fgl1 subjected to a steatosis or HCC experimental protocol. We found that mice deficient for Fgl1 in hepatocytes showed higher levels of plasma glucose, pronounced metabolic alterations, and liver injury when fed a western diet compared to their wild-type counterparts. However, both genotypes exhibited similar lipid deposition in the liver. Similarly, wild type aFASEB journal : official publication of the Federation of American Societies for Experimental BiologyAblation of Hepatocyte Derived-FGL1 Does Not Aggravate Metabolic Dysfunction-Associated Steatotic Liver Disease.PMC12365863ARF202209015711ANR‐16‐ACHN‐0002‐01 and ANR‐22‐CE14‐0076‐01715491ARCPOST‐DOC2022020004813ARCPOST-DOC2022020004813ANR-16-ACHN-0002-01 and ANR-22-CE14-0076-01Kautz LCannizzo LDaSilva JMartin CMPSotin MPersonnaz JGuillou HDesquesnes APerrier PfalseAblation of Hepatocyte Derived-FGL1 Does Not Aggravate Metabolic Dysfunction-Associated Steatotic Liver Disease.Metabolic dysfunction-associated steatotic liver disease (MASLD) begins with simple steatosis, which can progress to hepatocellular carcinoma (HCC). The pathogenesis of MASLD alters the secretion of hepatokines such as fibrinogen-like 1 (FGL1), a candidate mediator of liver steatosis and hyperglycemia. To investigate the contribution of FGL1 to liver diseases, we compared wild-type mice to mice with hepatocyte-specific deletion of Fgl1 subjected to a steatosis or HCC experimental protocol. We found that mice deficient for Fgl1 in hepatocytes showed higher levels of plasma glucose, pronounced metabolic alterations, and liver injury when fed a western diet compared to their wild-type counterparts. However, both genotypes exhibited similar lipid deposition in the liver. Similarly, wild type a2025-01-01T00:00:00Z2025 Aug2026-07-15T12:36:22.662Z2026-07-04T03:13:17.021ZS-EPMC123658634083276910.1096/fj.202501997R