Disturbed Gut-Liver axis indicating oral exposure to polystyrene microplastic potentially increases the risk of insulin resistance
[Display omitted] •We established an association between microplastics exposure and the occurrence of a disease.•Our findings highlight the health risks of a subset of the population with high exposure to microplastics.•Our study is the first to find an increased risk of insulin resistance contribut...
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Published in | Environment international Vol. 164; p. 107273 |
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Main Authors | , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Netherlands
Elsevier Ltd
01.06.2022
Elsevier |
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Abstract | [Display omitted]
•We established an association between microplastics exposure and the occurrence of a disease.•Our findings highlight the health risks of a subset of the population with high exposure to microplastics.•Our study is the first to find an increased risk of insulin resistance contributed by gut-liver axis.
Human uptake abundance of microplastics via various pathways, and they accumulate in human liver, kidney, gut and even placenta (especially with a diameter of 1 μm or less). Recent scientific studies have found that exposure to microplastics causes intestinal inflammation and liver metabolic disorder, but it remains largely unknown that whether the damage and inflammation may cause further development of severe diseases. In this study, we discovered one of such potential diseases that may be induced by the exposure to small-sized microplastics (with a diameter of 1 μm) performing a multi-organ and multi-omics study comprising metabolomics and microbiome approaches. Unlike other animal experiments, the dosing strategy was applied in mice according to the daily exposure of the highly exposed population, which was more environmentally relevant and reflective of real-world human exposure. Our studies on the gut-liver axis metabolism have shown that the crosstalk between the gut and liver ultimately leaded to insulin resistance and even diabetes. We proactively verified this hypothesis by measuring the levels of fasting blood glucose and fasting insulin, which were found significantly elevated in the mice with microplastics exposure. These results indicate the urgent need of large-scale cohort evaluation on epidemiology and prognosis of insulin resistance after microplastics exposure in future. |
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AbstractList | Human uptake abundance of microplastics via various pathways, and they accumulate in human liver, kidney, gut and even placenta (especially with a diameter of 1 μm or less). Recent scientific studies have found that exposure to microplastics causes intestinal inflammation and liver metabolic disorder, but it remains largely unknown that whether the damage and inflammation may cause further development of severe diseases. In this study, we discovered one of such potential diseases that may be induced by the exposure to small-sized microplastics (with a diameter of 1 μm) performing a multi-organ and multi-omics study comprising metabolomics and microbiome approaches. Unlike other animal experiments, the dosing strategy was applied in mice according to the daily exposure of the highly exposed population, which was more environmentally relevant and reflective of real-world human exposure. Our studies on the gut-liver axis metabolism have shown that the crosstalk between the gut and liver ultimately leaded to insulin resistance and even diabetes. We proactively verified this hypothesis by measuring the levels of fasting blood glucose and fasting insulin, which were found significantly elevated in the mice with microplastics exposure. These results indicate the urgent need of large-scale cohort evaluation on epidemiology and prognosis of insulin resistance after microplastics exposure in future. Human uptake abundance of microplastics via various pathways, and they accumulate in human liver, kidney, gut and even placenta (especially with a diameter of 1 μm or less). Recent scientific studies have found that exposure to microplastics causes intestinal inflammation and liver metabolic disorder, but it remains largely unknown that whether the damage and inflammation may cause further development of severe diseases. In this study, we discovered one of such potential diseases that may be induced by the exposure to small-sized microplastics (with a diameter of 1 μm) performing a multi-organ and multi-omics study comprising metabolomics and microbiome approaches. Unlike other animal experiments, the dosing strategy was applied in mice according to the daily exposure of the highly exposed population, which was more environmentally relevant and reflective of real-world human exposure. Our studies on the gut-liver axis metabolism have shown that the crosstalk between the gut and liver ultimately leaded to insulin resistance and even diabetes. We proactively verified this hypothesis by measuring the levels of fasting blood glucose and fasting insulin, which were found significantly elevated in the mice with microplastics exposure. These results indicate the urgent need of large-scale cohort evaluation on epidemiology and prognosis of insulin resistance after microplastics exposure in future.Human uptake abundance of microplastics via various pathways, and they accumulate in human liver, kidney, gut and even placenta (especially with a diameter of 1 μm or less). Recent scientific studies have found that exposure to microplastics causes intestinal inflammation and liver metabolic disorder, but it remains largely unknown that whether the damage and inflammation may cause further development of severe diseases. In this study, we discovered one of such potential diseases that may be induced by the exposure to small-sized microplastics (with a diameter of 1 μm) performing a multi-organ and multi-omics study comprising metabolomics and microbiome approaches. Unlike other animal experiments, the dosing strategy was applied in mice according to the daily exposure of the highly exposed population, which was more environmentally relevant and reflective of real-world human exposure. Our studies on the gut-liver axis metabolism have shown that the crosstalk between the gut and liver ultimately leaded to insulin resistance and even diabetes. We proactively verified this hypothesis by measuring the levels of fasting blood glucose and fasting insulin, which were found significantly elevated in the mice with microplastics exposure. These results indicate the urgent need of large-scale cohort evaluation on epidemiology and prognosis of insulin resistance after microplastics exposure in future. [Display omitted] •We established an association between microplastics exposure and the occurrence of a disease.•Our findings highlight the health risks of a subset of the population with high exposure to microplastics.•Our study is the first to find an increased risk of insulin resistance contributed by gut-liver axis. Human uptake abundance of microplastics via various pathways, and they accumulate in human liver, kidney, gut and even placenta (especially with a diameter of 1 μm or less). Recent scientific studies have found that exposure to microplastics causes intestinal inflammation and liver metabolic disorder, but it remains largely unknown that whether the damage and inflammation may cause further development of severe diseases. In this study, we discovered one of such potential diseases that may be induced by the exposure to small-sized microplastics (with a diameter of 1 μm) performing a multi-organ and multi-omics study comprising metabolomics and microbiome approaches. Unlike other animal experiments, the dosing strategy was applied in mice according to the daily exposure of the highly exposed population, which was more environmentally relevant and reflective of real-world human exposure. Our studies on the gut-liver axis metabolism have shown that the crosstalk between the gut and liver ultimately leaded to insulin resistance and even diabetes. We proactively verified this hypothesis by measuring the levels of fasting blood glucose and fasting insulin, which were found significantly elevated in the mice with microplastics exposure. These results indicate the urgent need of large-scale cohort evaluation on epidemiology and prognosis of insulin resistance after microplastics exposure in future. Human uptake abundance of microplastics via various pathways, and they accumulate in human liver, kidney, gut and even placenta (especially with a diameter of 1 μm or less). Recent scientific studies have found that exposure to microplastics causes intestinal inflammation and liver metabolic disorder, but it remains largely unknown that whether the damage and inflammation may cause further development of severe diseases. In this study, we discovered one of such potential diseases that may be induced by the exposure to small-sized microplastics (with a diameter of 1 μm) performing a multi-organ and multi-omics study comprising metabolomics and microbiome approaches. Unlike other animal experiments, the dosing strategy was applied in mice according to the daily exposure of the highly exposed population, which was more environmentally relevant and reflective of real-world human exposure. Our studies on the gut-liver axis metabolism have shown that the crosstalk between the gut and liver ultimately leaded to insulin resistance and even diabetes. We proactively verified this hypothesis by measuring the levels of fasting blood glucose and fasting insulin, which were found significantly elevated in the mice with microplastics exposure. These results indicate the urgent need of large-scale cohort evaluation on epidemiology and prognosis of insulin resistance after microplastics exposure in future. |
ArticleNumber | 107273 |
Author | Qu, Guangbo Wang, Shunhao Li, Min Shi, Jianbo Lv, Meilin Li, Zikang Tang, Gang Guo, Yunhe Han, Xiaohong Wu, Qi Wang, Yuanyuan Guo, Wei Wang, Ziniu Liu, Yaquan Shi, Chunzhen Yang, Xiaoxi Li, Junya Jiang, Guibin |
Author_xml | – sequence: 1 givenname: Chunzhen surname: Shi fullname: Shi, Chunzhen organization: College of Ecology and Environment, Beijing Technology and Business University, Beijing 100048, China – sequence: 2 givenname: Xiaohong surname: Han fullname: Han, Xiaohong organization: College of Ecology and Environment, Beijing Technology and Business University, Beijing 100048, China – sequence: 3 givenname: Wei surname: Guo fullname: Guo, Wei organization: College of Ecology and Environment, Beijing Technology and Business University, Beijing 100048, China – sequence: 4 givenname: Qi surname: Wu fullname: Wu, Qi organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 5 givenname: Xiaoxi surname: Yang fullname: Yang, Xiaoxi organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 6 givenname: Yuanyuan surname: Wang fullname: Wang, Yuanyuan organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 7 givenname: Gang surname: Tang fullname: Tang, Gang organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 8 givenname: Shunhao surname: Wang fullname: Wang, Shunhao organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 9 givenname: Ziniu surname: Wang fullname: Wang, Ziniu organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 10 givenname: Yaquan surname: Liu fullname: Liu, Yaquan organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 11 givenname: Min surname: Li fullname: Li, Min organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 12 givenname: Meilin surname: Lv fullname: Lv, Meilin organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 13 givenname: Yunhe surname: Guo fullname: Guo, Yunhe organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 14 givenname: Zikang surname: Li fullname: Li, Zikang organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 15 givenname: Junya surname: Li fullname: Li, Junya organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 16 givenname: Jianbo surname: Shi fullname: Shi, Jianbo organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 17 givenname: Guangbo surname: Qu fullname: Qu, Guangbo email: gbqu@rcees.ac.cn organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China – sequence: 18 givenname: Guibin surname: Jiang fullname: Jiang, Guibin organization: State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment Sciences, Chinese Academy of Sciences, Beijing 100085, China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35526298$$D View this record in MEDLINE/PubMed |
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Keywords | Metabolomics Insulin resistance Microplastic Gut-liver axis Microbiome |
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•We established an association between microplastics exposure and the occurrence of a disease.•Our findings highlight the health risks of a... Human uptake abundance of microplastics via various pathways, and they accumulate in human liver, kidney, gut and even placenta (especially with a diameter of... |
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SubjectTerms | at-risk population blood glucose diabetes environment Gut-liver axis humans inflammation insulin Insulin resistance intestines kidneys liver metabolism Metabolomics Microbiome Microplastic microplastics multiomics oral exposure placenta polystyrenes prognosis risk |
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Title | Disturbed Gut-Liver axis indicating oral exposure to polystyrene microplastic potentially increases the risk of insulin resistance |
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