Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver

Abstract Background Micro/nanoplastics (MNPs), as emerging environmental pollutants, are widely present in environments that are essential for human survival. They exist in vast quantities and possess stable properties, making them challenging to manage. Some reports indicated that there is a positi...

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Main Authors: Lijuan Chen, Guoyuan Sui, Jin Wu, Ning Li, Zhe Zhang, Ying Du, Meijun Lü, Xiaorui Yan, Guowei Pan, Lianqun Jia
Format: Article
Language:English
Published: BMC 2025-05-01
Series:Lipids in Health and Disease
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Online Access:https://doi.org/10.1186/s12944-025-02613-7
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author Lijuan Chen
Guoyuan Sui
Jin Wu
Ning Li
Zhe Zhang
Ying Du
Meijun Lü
Xiaorui Yan
Guowei Pan
Lianqun Jia
author_facet Lijuan Chen
Guoyuan Sui
Jin Wu
Ning Li
Zhe Zhang
Ying Du
Meijun Lü
Xiaorui Yan
Guowei Pan
Lianqun Jia
author_sort Lijuan Chen
collection DOAJ
description Abstract Background Micro/nanoplastics (MNPs), as emerging environmental pollutants, are widely present in environments that are essential for human survival. They exist in vast quantities and possess stable properties, making them challenging to manage. Some reports indicated that there is a positive correlation between the production of MNPs and the incidence of obesity. The liver serves as both the central hub for lipid metabolism and a prime target for MNPs toxicity. These studies revealed that MNPs can lead to increased hepatic lipid accumulation, suggesting that they may be potential obesogens. However, the specific metabolic changes and possible mechanisms involved remain to be elucidated. Methods This study focuses on the impact of nanoplastics (NPs) on liver lipid metabolism, using C57BL/6J mice (hereinafter referred to as C57 mice) as the research subjects, and exposing them to 100 nm NPs at 1000 µg/L continuously for 12 weeks. Results The study revealed that (1) NPs led to nondietary weight gain together with an increase in fat volume and mass in mice. (2) NPs significantly increased serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels, with notable differences between groups. Notably, NPs exposure induced opposing effects on serum lipid profiles, elevating high-density lipoprotein cholesterol (HDL-C) concentrations while suppressing triglyceride (TG) levels, though intergroup differences failed to reach statistical significance. (3) NPs caused multiple inflammatory responses in the liver, with significant lipid deposition. (4) Untargeted metabolomics analysis indicated that NPs exposure led to significant alterations in various lipid metabolites, particularly glycerophospholipids. Additionally, transcriptomics reveals that differentially expressed genes (DEGs) triggered by NPs exposure are predominantly involved in metabolic routes including lipid metabolism and cytochrome P450 (CYP). Taken together, these findings suggested that alterations in lipid metabolism resulting from NPs exposure may involve arachidonic acid metabolism. Phosphatidylcholine (PC) could be the key substance, and the CYP gene family (Cyp2c23, Cyp2c40) might be the critical genes regulating liver lipid metabolism during NPs exposure. Conclusions This study has demonstrated that NPs exposure induced obesity and hepatic lipid accumulation in male mice independently of food intake. The integrated omics data identified dysregulated PC metabolism and CYP gene family expression, suggesting their involvement in arachidonic acid-associated pathways. These findings provided preliminary mechanistic clues linking NP exposure to hepatic lipid metabolism dysregulation and helped to elucidate the adverse effects of NPs on liver lipid metabolism.
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spelling doaj-art-60a29d4763de42ff9fd1769b67f155e12025-08-20T02:03:32ZengBMCLipids in Health and Disease1476-511X2025-05-0124111810.1186/s12944-025-02613-7Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liverLijuan Chen0Guoyuan Sui1Jin Wu2Ning Li3Zhe Zhang4Ying Du5Meijun Lü6Xiaorui Yan7Guowei Pan8Lianqun Jia9Key Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese MedicineLiaoning University of Traditional Chinese MedicineKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese MedicineKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese MedicineKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese MedicineKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese MedicineKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese MedicineKey Laboratory of Ministry of Education for TCM Viscera-State Theory and Applications, Liaoning University of Traditional Chinese MedicineChina Medical UniversityLiaoning University of Traditional Chinese MedicineAbstract Background Micro/nanoplastics (MNPs), as emerging environmental pollutants, are widely present in environments that are essential for human survival. They exist in vast quantities and possess stable properties, making them challenging to manage. Some reports indicated that there is a positive correlation between the production of MNPs and the incidence of obesity. The liver serves as both the central hub for lipid metabolism and a prime target for MNPs toxicity. These studies revealed that MNPs can lead to increased hepatic lipid accumulation, suggesting that they may be potential obesogens. However, the specific metabolic changes and possible mechanisms involved remain to be elucidated. Methods This study focuses on the impact of nanoplastics (NPs) on liver lipid metabolism, using C57BL/6J mice (hereinafter referred to as C57 mice) as the research subjects, and exposing them to 100 nm NPs at 1000 µg/L continuously for 12 weeks. Results The study revealed that (1) NPs led to nondietary weight gain together with an increase in fat volume and mass in mice. (2) NPs significantly increased serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels, with notable differences between groups. Notably, NPs exposure induced opposing effects on serum lipid profiles, elevating high-density lipoprotein cholesterol (HDL-C) concentrations while suppressing triglyceride (TG) levels, though intergroup differences failed to reach statistical significance. (3) NPs caused multiple inflammatory responses in the liver, with significant lipid deposition. (4) Untargeted metabolomics analysis indicated that NPs exposure led to significant alterations in various lipid metabolites, particularly glycerophospholipids. Additionally, transcriptomics reveals that differentially expressed genes (DEGs) triggered by NPs exposure are predominantly involved in metabolic routes including lipid metabolism and cytochrome P450 (CYP). Taken together, these findings suggested that alterations in lipid metabolism resulting from NPs exposure may involve arachidonic acid metabolism. Phosphatidylcholine (PC) could be the key substance, and the CYP gene family (Cyp2c23, Cyp2c40) might be the critical genes regulating liver lipid metabolism during NPs exposure. Conclusions This study has demonstrated that NPs exposure induced obesity and hepatic lipid accumulation in male mice independently of food intake. The integrated omics data identified dysregulated PC metabolism and CYP gene family expression, suggesting their involvement in arachidonic acid-associated pathways. These findings provided preliminary mechanistic clues linking NP exposure to hepatic lipid metabolism dysregulation and helped to elucidate the adverse effects of NPs on liver lipid metabolism.https://doi.org/10.1186/s12944-025-02613-7Obesogenic factorsLipid accumulationArachidonic acid/metabolismPhosphatidylcholinesCytochrome P-450 enzyme system
spellingShingle Lijuan Chen
Guoyuan Sui
Jin Wu
Ning Li
Zhe Zhang
Ying Du
Meijun Lü
Xiaorui Yan
Guowei Pan
Lianqun Jia
Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
Lipids in Health and Disease
Obesogenic factors
Lipid accumulation
Arachidonic acid/metabolism
Phosphatidylcholines
Cytochrome P-450 enzyme system
title Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
title_full Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
title_fullStr Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
title_full_unstemmed Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
title_short Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
title_sort untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
topic Obesogenic factors
Lipid accumulation
Arachidonic acid/metabolism
Phosphatidylcholines
Cytochrome P-450 enzyme system
url https://doi.org/10.1186/s12944-025-02613-7
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