Ablation of Hepatocyte Derived-FGL1 Does Not Aggravate Metabolic Dysfunction-Associated Steatotic Liver Disease.

ABSTRACT: 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 a

SUBMITTER: Personnaz J 

PROVIDER: S-EPMC12365863 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature