ArticleBMC medicine2026
DNA hypermethylation of choline kinases drives blockage of choline-phosphatidylcholine biosynthesis: lipidomic biomarkers and epigenetic insights of hepatic steatosis induced by arsenic.
Article in BMC medicine, 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
backgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) is a global public health issue. Beyond genetic variation and behavior-related risk factors, inorganic arsenic, with a broad exposed population, serves as a critical environmental risk factor for MASLD. While hepatic steatosis has been identified as the initiating event of arsenic-induced MASLD, its effect biomarkers and underlying mechanisms remain unclear, a knowledge gap that is crucial for risk monitoring and early intervention. This study aims to identify the biomarkers and potential epigenetic mechanisms of arsenic-induced hepatic steatosis from the perspective of lipid metabolism.
methodsThis study recruited patients with arsenic-poisoned fatty liver and used lipid metabolomics to evaluate serum lipid metabolic profile alterations in these patients. Concurrently, a mouse model exposed to environmentally relevant doses of sodium arsenite (NaAsO₂) was established, with liver lipid metabolomics applied to assess arsenic's impact on lipid metabolic pathways in hepatic steatosis. Furthermore, by combining this mouse model with an in vitro model of NaAsO₂-induced lipid accumulation in hepatocytes, methods including RT-qPCR, Western blotting, and MassARRAY DNA methylation quantification were employed to explore the potential mechanism of arsenic-induced hepatic lipid metabolism disorders. Additionally, in vitro intervention models with phosphatidylcholine (PC) supplements and DNA methyltransferase inhibitors were used to validate this mechanism.
resultsPopulation studies showed that reduced PC levels are a significant feature of serum lipid profiles in arsenic-poisoned fatty liver patients. The accuracy of distinguishing this disease via decreased PC molecules was 83.33%. Mouse liver lipid metabolomics further revealed this PC collapse results from arsenic inhibiting hepatic choline-to-PC synthesis. Notably, mouse and in vitro studies showed arsenic upregulates DNMT1 and inhibits TET1 and TET2, inducing Chkα/Chkβ promoter hypermethylation to suppress choline-PC synthesis. This reduced triglyceride transporter levels (very-low-density lipoprotein), causing intrahepatic lipid accumulation. Supplementing PC or using DNA methyltransferase inhibitors alleviated these adverse effects in vitro.
conclusionsThis study innovatively identifies reduced serum-specific PC molecules as a potential risk marker for arsenic-induced hepatic steatosis. Chkα/Chkβ hypermethylation-mediated PC synthesis disorder is the key mechanism of arsenic-induced hepatic steatosis, and DNMT1, TET1, and TET2 dysregulation may underlie this hypermethylation. PC supplementation or epigenetic correction shows intervention potential.
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