G3BP1, a stress granule core protein, ameliorates metabolic dysfunction‐associated fatty liver disease by attenuating hepatocyte lipid deposition

Diabetes Obesity and Metabolism, Journal Year: 2025, Volume and Issue: unknown

Published: April 15, 2025

Abstract Aim Abnormal lipid accumulation is an important cause of metabolic dysfunction‐associated fatty liver disease (MAFLD) progression and can induce several stress responses within cells. This study the first to explore role molecular mechanism granules (SGs) in MAFLD. Methods A gene knock‐down model G3BP1, a core SG molecule mice HepG2 cells, was constructed SGs MAFLD induced vivo by high‐fat diet or vitro palmitic acid (PA). included phenotyping; western blotting; qPCR; immunofluorescence, haematoxylin/eosin masson staining. The downstream molecules G3BP1 its specific were screened using RNA sequencing (RNA‐seq). Results TIA1 expression upregulated diet‐fed mouse tissues PA‐induced two showed significantly increased colocalisation. slightly livers obese but not lean mice. deficiency aggravated deposition insulin resistance mice, this phenotype confirmed hepatocytes. RNA‐seq demonstrated that slowed down inhibiting APOC3, possibly through mechanistic suppression APOC3 entry into nucleus. Conclusion reveals for time protective Specifically, knocking acid‐induced may involve nuclear APOC3. These findings provide new therapeutic direction

Language: Английский

New insights into the mechanism of T-2 toxin cytotoxicity: stress granules inhibit the mTORC2/AKT signaling pathway

Food Bioscience, Journal Year: 2025, Volume and Issue: unknown, P. 106806 - 106806

Published: May 1, 2025

Language: Английский