ArticleMolecular metabolism2026
High salt supplementation of a MASH-inducing diet causes lean MASH phenotype with increased hepatic urea cycle activity and EIF5A hypusination.
Article in Molecular metabolism, 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
backgroundMASLD/MASH can occur in lean individuals; however, the environmental triggers and molecular mechanisms underlying lean MASH are unclear, and suitable animal models are lacking.
resultsMice fed a Western diet with liquid fructose (WDF) develops obesity and MASH (obese MASH). In contrast, high salt supplementation of WDF (HSWDF) produced a lean MASH phenotype with reduced steatosis but induced significant inflammation and fibrosis (lean MASH). In WDF-induced obese MASH, we observed decreased urea cycle activity and flux, along with reduced eukaryotic translation initiation factor 5 A hypusination (EIF5AH) and mitochondrial biosynthesis. High salt supplementation of WDF unexpectedly ameliorated these alterations, enhanced hepatic fatty acid oxidation and reduced hepatosteatosis. However, single-cell sequencing revealed that dietary high salt was associated with pro-inflammatory responses in hepatic immune cell subpopulations.
conclusionsIn summary, we have established a dietary mouse model of lean MASH that differs from obese-MASH in hepatic urea cycle, mitochondrial protein synthesis, and immune cell activation, providing new mechanistic insight into lean MASH.
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