ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2026
Ethanol reshapes FFC-driven steatohepatitis through time-dependent fibrosis and lipid-droplet remodeling.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Metabolic dysfunction and alcohol exposure drive steatotic liver disease, yet how ethanol intersects with metabolic steatohepatitis remains incompletely defined. Our iterative model examined how ethanol ingestion alters high-fat, -fructose, and -cholesterol (FFC)-driven liver injury, identifying metabolic dysfunction and alcohol-associated liver disease (MetALD)-relevant features. A pilot study in male and female C57BL/6J mice compared chow diet (CD), FFC, CD + ethanol (E), and FFC + E on high-glucose/fructose (sugar) water (SW) at 6, 16, and 24 wk. A redesigned study lowered glucose/fructose exposure, modified ethanol acclimation, and tested five male cohorts: CD, CD + SW, FFC + SW, CD + SW + E, FFC + SW + E, at 16 and 24 wk. In the pilot study, FFC-dominant hepatomegaly, aminotransferase elevation, steatosis, chemokine induction, and fibrosis, without additive ethanol effects, were observed. In the redesigned model, FFC drove weight gain, hepatomegaly, steatosis, aminotransferase elevation, and chemokine (C-C motif) ligand 2 (
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