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Updated: May 26, 2026

Collection of Alfalfa Root Exudates to Study the Impact of Di(2-ethylhexyl) Phthalate on Metabolite Production
Published on: June 2, 2023
Pre-existing liver dysfunction modulates di-(2-ethylhexyl) phthalate (DEHP)-associated biological responses through
Mingzhu Wu1, Shucong Chen1, Wencheng Guo1
1MOE Key Laboratory of Pollution Processes and Environmental Criteria, College of Environmental Science and Engineering, Nankai University, Tianjin, 300350, China.
Metabolic dysfunction-associated steatotic liver disease (MASLD) may worsen responses to the plasticizer di-(2-ethylhexyl) phthalate (DEHP). Fatty liver disease alters DEHP metabolism and gut bacteria, impacting host metabolic and inflammatory pathways.
Area of Science:
- Environmental Health
- Metabolomics
- Toxicology
Background:
- Metabolic conditions can alter responses to environmental pollutants.
- Metabolic dysfunction-associated steatotic liver disease (MASLD) and its impact on chemical exposure are underexplored.
- Di-(2-ethylhexyl) phthalate (DEHP) is a common plasticizer with potential health effects.
Purpose of the Study:
- To investigate if pre-existing MASLD alters biological responses to DEHP.
- To examine the association between fatty liver status and DEHP metabolite profiles in humans.
- To explore the effects of DEHP exposure on metabolism and the gut microbiome in a rat model with hepatic lipid accumulation.
Main Methods:
- Human cohort study analyzing urinary DEHP metabolites.
- Rat model with multi-omics approaches (metabolomics, transcriptomics, gut microbiome analysis).
- Assessment of DEHP burden, tissue distribution, metabolic pathways, gene expression, and microbial community shifts.
Main Results:
- Fatty liver status correlated with higher proportions of bioactive mono-(2-ethylhexyl) phthalate in humans.
- MASLD model showed increased systemic DEHP burden, altered tissue distribution (liver, intestine), and metabolic pathway perturbations.
- DEHP exposure exacerbated gut microbiota dysbiosis and upregulated hepatic genes involved in lipogenesis and cholesterol metabolism.
- Integrative analysis suggested coordinated alterations in microbiome, metabolome, and hepatic transcriptome via the gut-liver axis.
Conclusions:
- Pre-existing MASLD may exacerbate DEHP-associated biological responses.
- The gut-liver axis plays a role in mediating these exacerbated responses.
- Host metabolic status is a critical factor in understanding chemical-associated biological effects.
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