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Gut dysbiosis is linked to severe steatosis and enhances its diagnostic performance in MASLD.
eGastroenterology
August 2025
Serviço de Endocrinologia, Diabetes e Metabolismo, ULS São João, Porto, Portugal.
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease globally, with rising prevalence linked to metabolic syndrome (MetS). Excessive liver fat accumulation (steatosis) worsens disease progression and MASLD prognosis. Moreover, gut microbiota dysbiosis might promote steatosis, accelerating the disease progression to severe stages.
View Article and Find Full Text PDFRegulatory Role and Biomarker Potential of Gut Microbiota Metabolites in the Progression of Metabolic dysfunction-associated steatotic liver disease (MASLD) to Hepatocellular Carcinoma (HCC).
Clin Transl Gastroenterol
September 2025
Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan, 030032, China.
Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide. It is now updated as metabolic dysfunction-associated steatotic liver disease (MASLD). The progression of MASLD to hepatocellular carcinoma (HCC) involves complex mechanisms, with the gut microbiota and its metabolites playing a pivotal role in this transformation through the "gut-liver axis.
View Article and Find Full Text PDFMetabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease globally. Disruptions in iron metabolism and mitochondrial oxidative function may cooperatively contribute to its pathogenesis. Ferredoxin reductase (FDXR), a mitochondrial flavoprotein, plays a critical role in mitochondrial respiratory supercomplex formation and iron-sulfur cluster biosynthesis-both essential for efficient oxidative metabolism.
View Article and Find Full Text PDFCideb knockdown in mice increases mitochondrial fat oxidation and reverses hepatic steatosis and insulin resistance by the plasma membrane sn-1,2-DAGs-PKCε-insulin receptor kinase pathway.
Diabetologia
September 2025
Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
Aims/hypothesis: CIDEB (cell death-inducing DFF45-like effector B) deficiency is associated with a reduced incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) in humans; however, the underlying mechanism responsible for this protective effect remains unclear.
Methods: C57BL/6J male mice were fed a high-fat diet (HFD) to recapitulate key aspects of MASLD and hepatic insulin resistance. Cideb knockdown (KD) was achieved using a 2'-O-methoxyethyl (MOE) antisense oligonucleotide (ASO).
Electronic decision aids enhance management of primary care patients with steatotic liver disease: Proof of concept pilot study.
Hepatol Commun
September 2025
Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Background: The approach to appropriate risk stratification for metabolic dysfunction-associated steatotic liver disease (MASLD) is variable, and the adoption of non-invasive liver disease assessments in clinical practice is suboptimal. In this study, we implemented an electronic decision support tool for primary care patients with MASLD to assess its influence on linkage to care.
Methods: We performed a prospective, before-and-after pilot study in which post-implementation providers were presented with an electronic decision aid automating non-invasive liver disease assessments with the Fibrosis-4 score and providing individualized, guideline-directed recommendations.