Evidence map›Paper›PMID 41177821›Full record

ArticleMetabolomics : Official journal of the Metabolomic Society2025

Increased 1-deoxysphingolipids caused by an altered plasma alanine to serine ratio are associated with metabolic dysfunction-associated steatotic liver disease (MASLD).

F Wipfli, M A Lone, A von Eckardstein, A Verrijken, S Francque, J Weyler, L Van Gaal, B Staels, T Hornemann

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Article in Metabolomics : Official journal of the Metabolomic Society, 2025. 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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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

F WipfliInstitute of Clinical Chemistry, University Hospital Zurich and University of Zurich, 8091, Zurich, Switzerland.
M A LoneInstitute of Clinical Chemistry, University Hospital Zurich and University of Zurich, 8091, Zurich, Switzerland.ORCID http://orcid.org/0000-0001-9710-775X
A von EckardsteinInstitute of Clinical Chemistry, University Hospital Zurich and University of Zurich, 8091, Zurich, Switzerland.
A VerrijkenDepartment of Gastroenterology Hepatology, Antwerp University Hospital, Drie Eikenstraat 655, B-2650, Edegem, Belgium.
S FrancqueDepartment of Gastroenterology Hepatology, Antwerp University Hospital, Drie Eikenstraat 655, B-2650, Edegem, Belgium.
J WeylerDepartment of Gastroenterology Hepatology, Antwerp University Hospital, Drie Eikenstraat 655, B-2650, Edegem, Belgium.
L Van GaalDepartment of Gastroenterology Hepatology, Antwerp University Hospital, Drie Eikenstraat 655, B-2650, Edegem, Belgium.
B StaelsUniversity of Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011- EGID, Lille, France.
T HornemannInstitute of Clinical Chemistry, University Hospital Zurich and University of Zurich, 8091, Zurich, Switzerland. thorsten.hornemann@usz.ch.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) (formerly Non-Alcoholic Fatty Liver Disease, NAFLD) encompasses a spectrum of metabolic disorders ranging from isolated steatosis to Metabolic Dysfunction-Associated Steatohepatitis (MASH), potentially progressing to cirrhosis and hepatocellular carcinoma (HCC). In this study, we investigated metabolic changes in MASLD by analysing plasma lipidomics and metabolomics profiles from 315 biopsy-characterized patients. We observed significant alterations in alanine/serine (ala/ser) ratio, 1-deoxysphingolipids, alanine aminotransferase (ALT), and waist/hip ratio (whr) between patients with and without MASH. These findings highlight a close interplay between amino acid metabolism and sphingolipid biosynthesis in MASLD progression. The shift in ala/ser ratio particularly distinguished non-MASH from borderline MASH patients, suggesting that early metabolic disruptions precede overt liver damage. Additionally, elevated branched-chain and aromatic amino acids correlated with steatosis severity, reinforcing the central role of amino acid dysregulation in MASLD. While a simple model combining ALT, ala/ser ratio, and whr showed some potential to support risk stratification, the primary significance of our findings lies in the mechanistic insights into metabolic dysfunction. In conclusion, this study emphasizes the importance of metabolic network alterations in MASLD and points toward future opportunities for both mechanistic research and the development of supportive diagnostic strategies.

Indexed as

AlanineNon-alcoholic Fatty Liver DiseaseSerineSphingolipidsAdultAgedAlanine TransaminaseFemaleHumansMaleMetabolomicsMiddle AgedAlanineAlanine TransaminaseSerineSphingolipids

Identifiers

PMID41177821
PMCPMC12580439

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.