Evidence map›Paper›PMID 40726434›Full record

ArticleDiabetes, obesity & metabolism2025

Higher plasma dicarbonyl levels are associated with liver fibrosis in obese individuals.

Oluwatomisono I Akinrimisi, Mijra Koning, Jean L J M Scheijen, Abraham S Meijnikman, Daniko P Sindhunata, Sjoerd Bruin, Arnold van de Laar, Rutger Franken, Yair Acherman, Victor E A Gerdes and 3 more

Abstract read
In one paragraph

Article in Diabetes, obesity & metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Oluwatomisono I AkinrimisiDepartment of Experimental Vascular & Internal Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.ORCID 0009-0005-0759-9276
Mijra KoningDepartment of Experimental Vascular & Internal Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Jean L J M ScheijenCARIM, School for Cardiovascular Diseases, Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.ORCID 0000-0002-1268-2286
Abraham S MeijnikmanDepartment of Experimental Vascular & Internal Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.ORCID 0000-0001-8653-6591
Daniko P SindhunataDepartment of Experimental Vascular & Internal Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Sjoerd BruinTytgat Institute for Liver and Intestinal Research, Amsterdam University Medical Center, Amsterdam, The Netherlands.
Arnold van de LaarTytgat Institute for Liver and Intestinal Research, Amsterdam University Medical Center, Amsterdam, The Netherlands.
Rutger FrankenTytgat Institute for Liver and Intestinal Research, Amsterdam University Medical Center, Amsterdam, The Netherlands.
Yair AchermanTytgat Institute for Liver and Intestinal Research, Amsterdam University Medical Center, Amsterdam, The Netherlands.ORCID 0000-0003-2787-8596
Victor E A GerdesDepartment of Experimental Vascular & Internal Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Max NieuwdorpDepartment of Experimental Vascular & Internal Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.ORCID 0000-0002-1926-7659
Casper G SchalkwijkCARIM, School for Cardiovascular Diseases, Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.ORCID 0000-0003-0190-2690
Nordin M J HanssenDepartment of Experimental Vascular & Internal Medicine, Amsterdam University Medical Centers, Amsterdam, The Netherlands.ORCID 0000-0001-9541-7244

Funding

Dutch Gastroenterology and Hepatology FoundationERC Advanced Grant 101141346NWO VICI grant 2020 09150182010020Senior Clinical Dekker grant by the Dutch Heart Foundation 2021T055VENI grant 2023 09150162310148ZONMW-VIDI grant 2023 09150172210019
6 · The paper itself

Abstract

introductionMethylglyoxal (MGO) is a very reactive compound that modifies proteins, forming advanced glycation end products (AGEs) and activating inflammatory pathways. Elevated MGO levels have been linked to various diseases, including type 2 diabetes and atherosclerosis. However, the role of MGO and other glycating agents in the progression of liver fibrosis in the setting of metabolic dysfunction associated steatotic liver disease (MASLD) is poorly understood.

methodsThis study explores the relationship between plasma MGO levels and related dicarbonyls (glyoxal (GO) and 3-deoxyglucosone (3-DG)), which are measured using ultra-high-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS), and liver fibrosis assessed via histological liver biopsy scoring and the Fibrosis-4 (FIB-4) Index. The study population comprised 264 severely obese individuals due to undergo bariatric surgery, a subset from the BARIA cohort (22% type 2 diabetes; 77% females; median age 47 (IQR: 39-54 years); BMI 39 (IQR: 36-41 kg/m

resultsMGO levels were significantly higher in individuals with type 2 diabetes compared with individuals without type 2 diabetes, with a median of 288 nmol/L (257-334 nmol/L) and 238 (212-279 nmol/L) respectively. MGO levels were higher in males compared with females, with a median of 267 (236-301 nmol/L) and 245 (214-288 nmol/L) respectively. Similar results were found for GO and 3DG. Higher plasma MGO, GO and 3DG levels were significantly associated with the FIB-4 Index (MGO, rho = 0.21, p < 0.01), (GO, rho = 0.29, p < 0.01), (3DG, rho = 0.25, p < 0.05). Using linear regression models, the association between MGO and the FIB-4 Index remained significant after adjustment for age (years), sex, BMI, sub-cohort, smoking status, alcohol consumption, hypertension, HOMA-IR, HbA1c and fasting glucose levels. Using ordinal logistic regression models, MGO and GO were also associated with liver fibrosis scoring from biopsy before and after adjustment for confounders (Age (years), sex, BMI, sub-cohort, smoking status, alcohol consumption, hypertension, HOMA-IR, HbA1c and fasting glucose levels). Notably, the relationships remained significant in individuals without type 2 diabetes and after adjusting for HbA1c and fasting glucose levels. No significant associations were observed between MGO, GO, or 3DG and steatosis or inflammation histology scores after adjustment for confounders.

conclusionThis study shows the potential role of dicarbonyl stress, particularly MGO, in liver fibrosis among obese individuals, highlighting its significance as an independent contributor to liver damage and a potential therapeutic target.

Indexed as

DeoxyglucoseGlyoxalLiver CirrhosisObesityPyruvaldehydeAdultBiomarkersDiabetes Mellitus, Type 2FemaleHumansLiverMaleMiddle Aged3-deoxyglucosoneBiomarkersDeoxyglucoseGlyoxalPyruvaldehydedicarbonylsfibrosislivermethylglyoxaltype 2 diabetes

Identifiers

PMID40726434
PMCPMC12409227

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LicenceCC BY-NC-ND
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Registered trials

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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.