ArticlebioRxiv : the preprint server for biology2026
Sulfur amino acid restriction prevents S-adenosylmethionine-driven liver steatosis, hepatocellular carcinoma, and metabolic remodeling in high-fat-fed GNMT-null mice.
Article in bioRxiv : the preprint server for biology, 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
The expression of glycine N-methyltransferase (GNMT), a critical regulator of S-adenosylmethionine (SAM) levels, is down-regulated in humans with metabolic dysfunction-associated steatotic liver disease (MASLD) and hepatocellular carcinoma (HCC). In low-fat-fed mice, GNMT knockout (KO) induces liver steatosis that progresses to HCC. This is accompanied by increased SAM and a shunting of tricarboxylic acid (TCA) cycle intermediates away from gluconeogenesis to other biosynthetic pathways that support lipid accretion and tumorigenesis. The objective of this study was to test whether this metabolic remodeling persists in GNMT KO mice with diet-induced obesity and to determine if the liver pathophysiology and metabolic dysregulation are dependent on elevated SAM. To accomplish this, GNMT KO mice and wild-type (WT) littermates were fed a high-fat control or high-fat sulfur amino acid restricted (SAAR) diet to mitigate SAM accumulation.
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