ArticleLiver international : official journal of the International Association for the Study of the Liver2026
Urinary Volatile Organic Compound Metabolites Are Associated With MASLD/MASH in Humans and Induce Steatosis in Liver Organoids.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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.
Who cites it
1 citing paper in PubMed.
- Urinary Volatile Organic Compound Metabolites Are Associated With MASLD/MASH in Humans and Induce Steatosis in Liver Organoids.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundVolatile organic compound (VOC) exposure is an environmental health concern and could, through the liver exposome, be associated with metabolic dysfunction associated steatotic liver disease (MASLD) progression.
methodsWe analysed NHANES 2017-2020, a U.S. population-based cohort with controlled attenuation parameter (CAP), liver stiffness measurement (LSM) and urinary VOC metabolites. Participants with viral hepatitis, excess alcohol use or missing urine creatinine were excluded. MASLD was defined as CAP ≥ 275 dB/m with metabolic dysfunction, at-risk MASH as FAST ≥ 0.35 and increased LSM as ≥ 8 kPa. Weighted quantile sum (WQS) regression assessed associations between VOC metabolites and outcomes, adjusting for age, sex, smoking and alcohol. Phenylglyoxylic acid (PGA) and mandelic acid (MA) were further examined using logistic regression for the MA/(MA and PGA) ratio and human liver organoids.
resultsThe cohort comprised 2004 participants (41.4% MASLD, 5.4% at-risk MASH, 9.7% LSM ≥ 8 kPa). Higher VOC metabolite levels were associated with increased risk of MASLD (aOR 1.47 per quartile, 95% CI 1.06-2.04) and at-risk MASH (aOR 2.69 per quartile, 95% CI 1.23-5.87), primarily driven by N-Acetyl-S-(2-carboxyethyl)-L-cysteine (CEMA) and N-Acetyl-S-(3-hydroxy-1-methylpropyl)-L-cysteine (HMPMA), with inverse associations driven by PGA. No significant associations were found for increased LSM, yet a higher MA/(MA + PGA) ratio was associated with increased risk for at-risk MASH and LSM ≥ 8 kPa. In human liver organoids, PGA exposure increased lipid droplet number and size.
conclusionUrinary VOC metabolites show distinct associations with MASLD and at-risk MASH in the general population. CEMA and HMPMA were associated with increased risk, consistent with prior links to metabolic dysfunction. PGA induced steatosis in liver organoids, suggesting poor metabolising of styrene and ethylbenzene and intracellular PGA accumulation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.