ArticleHepatology communications2025
VLDL lipidomics reveals hepatocellular lipidome changes in metabolic dysfunction-associated steatotic liver disease.
Article in Hepatology communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Semaglutide improves markers of cardiovascular risk in people with HIV.AIDS (London, England) · 2026Trial
- Broad-Coverage Lipidomics Reveals Temporal Lipid Remodeling and Candidate Serum Biomarkers After Acute Spinal Cord Injury in Rats.Biomedicines · 2026Article
- Clinical clustering identifies MASLD subtypes with distinct longitudinal cardiovascular risks and lipidomic profiles.Hepatology international · 2026Article
- Plasma metabolic signatures of healthy dietary patterns and risk of metabolic dysfunction-associated steatotic liver disease and cirrhosis.Hepatology international · 2026Article
- Mechanisms of postpartum metabolic dysfunction-associated steatotic liver disease in women with a history of gestational diabetes mellitus.Endocrine connections · 2026Review
- Choline Deficiency Drives the Inflammation-Fibrosis Cascade: A Spatiotemporal Atlas of Hepatic Injury from Weeks 6 to 10.Antioxidants (Basel, Switzerland) · 2026Article
- Role of activity and fibrosis in the MASLD atherogenic momentum through advanced lipidomics.PloS one · 2026Article
- Deoxyguanosine kinase deficiency couples purine metabolism to innate immune activation and lipid accumulation in hepatocytes.Frontiers in immunology · 2026Article
- Adipocyte death promotes hepatic infiltration of S100A8+ macrophages and steatotic liver disease progression in mice.The Journal of clinical investigation · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundThe production of VLDL is one of the primary mechanisms through which liver cells regulate intracellular lipid homeostasis. We hypothesize that the disease characteristics of metabolic dysfunction-associated steatotic liver disease (MASLD) differentially impact VLDL lipid composition. This study comprehensively examines the relationship between VLDL-lipidome and MASLD histology and disease-associated genetics, aiming to define MASLD-related VLDL changes.
methodsWe performed untargeted lipidomics on serum VLDL particles in a cohort of biopsy-proven MASLD patients to examine the relationship between VLDL-lipidome and MASLD disease features as well as MASLD-related genetic variants.
resultsAmong 1514 detected lipid species in VLDL, triglyceride (TG), phosphatidylcholine (PC), and ceramide (Cer) were the top classes. Moderate to severe hepatic steatosis was associated an increase in VLDL-TG, especially those with palmitic acid (C16:0). A unified acyl chain distribution analysis revealed that steatosis was associated with increases in TGs with saturated and monounsaturated fatty acyl chains, but decreases in polyunsaturated fatty acyl chains, a pattern that was not mirrored in acyl chains from VLDL-PC or VLDL-Cer. Lobular inflammation was associated with reductions in lipids with polyunsaturated acyl chains, particularly docosahexaenoic acid (C22:6). Meanwhile, patients with advanced liver fibrosis (stages 3-4) had reductions in VLDL-TGs with both saturated and polyunsaturated acyl chains and overall enrichment in Cer species. Furthermore, MASLD-associated genetic variants in PNPLA3, TM6SF2, GPAM, HSD17B13, and MTARC1 demonstrated distinct VLDL-lipidomic signatures in keeping with their biology in lipoprotein metabolism.
conclusionsHepatic steatosis and liver fibrosis in MASLD are associated with distinct VLDL-lipidomic signatures, respectively. This relationship is further modified by MASLD-genetics, suggesting a differential impact of pathogenic features on hepatocellular lipid homeostasis.
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