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Mobilization of the Environmental Toxicant Chlorpyrifos during Weight Loss and Its Impact on Liver and Adipose Tissue Metabolism in Mice.

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Title: Mobilization of the Environmental Toxicant Chlorpyrifos during Weight Loss and Its Impact on Liver and Adipose Tissue Metabolism in Mice.
Authors: Yifan Xiang1, Gaojian Tang1, Xiaohu Hu1,2, Xiaoxiao Yu1,3, Yanrong Feng1, Zhongzuo Huang1, Yicheng Luo1, Zongyou Jiang1, Yue Lv1,2, Xiaoying Sun1, Yan Zhang1, Long Cheng1, Yu Xin1, Yuxin Qian1, Boyu Li1, Bo Wang1 wangbo123@cau.edu.cn
Source: Environmental Health Perspectives. Jul2026, Vol. 134 Issue 3, p274-288. 15p.
Subjects: Weight loss, High performance liquid chromatography, Glucose intolerance, Adipose tissues, Homeostasis, Research funding, Statistical hypothesis testing, Glucose tolerance tests, Fisher exact test, Brain, Reverse transcriptase polymerase chain reaction, AMP-activated protein kinases, Cellular signal transduction, Organothiophosphorus compounds, Energy metabolism, Mice, Experimental design, Fibrosis, Genes, Metabolites, Pollutants, Animal experimentation, Western immunoblotting, One-way analysis of variance, Liver, Inflammation
Geographic Terms: China
Abstract: BACKGROUND: Fat-soluble toxicants, such as chlorpyrifos (CPF) can accumulate in adipose tissue and the liver. During weight loss, these compounds may be released into the circulation, but the metabolic consequences of this mobilization remain poorly understood. OBJECTIVES: This study aimed to investigate the mobilization of CPF during weight loss and its effects on liver health and adipose tissue metabolism in mice. METHODS: C57BL/6J mice were fed a high-fat diet (HFD) or a low-fat diet (LFD) and exposed to 2 mg/kg BW/day CPF by oral gavage. Weight loss was induced by β3-adrenergic stimulation (CL316243) or treadmill exercise for 4 or 10 weeks. CPF was quantified in serum and tissues using HPLC. Tissue histology, expression of genes related to CPF metabolism, liver injury markers, and metabolic protein levels were assessed. RESULTS: CPF-exposed LFD mice showed more severe liver fibrosis and adipose inflammation than did their HFD counterparts. While obese mice had lower adipose CPF concentrations, they showed higher hepatic accumulation. CPF-exposed weight loss mice had higher levels of CPF in adipose tissue, liver, and brain and higher expression of CPF metabolism-related genes, including Paraoxinase-1 and cytochrome P450 genes, and greater glucose intolerance compared to their counterparts without CPF administration. Molecular analyses revealed suppressed AMPK signaling and P62 accumulation, indicating mitophagy disruption in CPF-exposed mice after weight loss. These effects occurred even at human-relevant low doses (0.45 mg/kg of BW/day) and persisted across sexes. DISCUSSION: Weight loss mobilizes CPF and its metabolites from fat stores, leading to tissue accumulation and damage. Even low-dose exposure contributes to hepatic and metabolic disruption in mice, highlighting the potential risk of toxicant mobilization during fat reduction. [ABSTRACT FROM AUTHOR]
Copyright of Environmental Health Perspectives is the property of National Institute of Environmental Health Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Mobilization of the Environmental Toxicant Chlorpyrifos during Weight Loss and Its Impact on Liver and Adipose Tissue Metabolism in Mice.
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  Data: <searchLink fieldCode="AR" term="%22Yifan+Xiang%22">Yifan Xiang</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Gaojian+Tang%22">Gaojian Tang</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Xiaohu+Hu%22">Xiaohu Hu</searchLink><relatesTo>1,2</relatesTo><br /><searchLink fieldCode="AR" term="%22Xiaoxiao+Yu%22">Xiaoxiao Yu</searchLink><relatesTo>1,3</relatesTo><br /><searchLink fieldCode="AR" term="%22Yanrong+Feng%22">Yanrong Feng</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Zhongzuo+Huang%22">Zhongzuo Huang</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Yicheng+Luo%22">Yicheng Luo</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Zongyou+Jiang%22">Zongyou Jiang</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Yue+Lv%22">Yue Lv</searchLink><relatesTo>1,2</relatesTo><br /><searchLink fieldCode="AR" term="%22Xiaoying+Sun%22">Xiaoying Sun</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Yan+Zhang%22">Yan Zhang</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Long+Cheng%22">Long Cheng</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Yu+Xin%22">Yu Xin</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Yuxin+Qian%22">Yuxin Qian</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Boyu+Li%22">Boyu Li</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Bo+Wang%22">Bo Wang</searchLink><relatesTo>1</relatesTo><i> wangbo123@cau.edu.cn</i>
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  Data: <searchLink fieldCode="JN" term="%22Environmental+Health+Perspectives%22">Environmental Health Perspectives</searchLink>. Jul2026, Vol. 134 Issue 3, p274-288. 15p.
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  Data: <searchLink fieldCode="DE" term="%22Weight+loss%22">Weight loss</searchLink><br /><searchLink fieldCode="DE" term="%22High+performance+liquid+chromatography%22">High performance liquid chromatography</searchLink><br /><searchLink fieldCode="DE" term="%22Glucose+intolerance%22">Glucose intolerance</searchLink><br /><searchLink fieldCode="DE" term="%22Adipose+tissues%22">Adipose tissues</searchLink><br /><searchLink fieldCode="DE" term="%22Homeostasis%22">Homeostasis</searchLink><br /><searchLink fieldCode="DE" term="%22Research+funding%22">Research funding</searchLink><br /><searchLink fieldCode="DE" term="%22Statistical+hypothesis+testing%22">Statistical hypothesis testing</searchLink><br /><searchLink fieldCode="DE" term="%22Glucose+tolerance+tests%22">Glucose tolerance tests</searchLink><br /><searchLink fieldCode="DE" term="%22Fisher+exact+test%22">Fisher exact test</searchLink><br /><searchLink fieldCode="DE" term="%22Brain%22">Brain</searchLink><br /><searchLink fieldCode="DE" term="%22Reverse+transcriptase+polymerase+chain+reaction%22">Reverse transcriptase polymerase chain reaction</searchLink><br /><searchLink fieldCode="DE" term="%22AMP-activated+protein+kinases%22">AMP-activated protein kinases</searchLink><br /><searchLink fieldCode="DE" term="%22Cellular+signal+transduction%22">Cellular signal transduction</searchLink><br /><searchLink fieldCode="DE" term="%22Organothiophosphorus+compounds%22">Organothiophosphorus compounds</searchLink><br /><searchLink fieldCode="DE" term="%22Energy+metabolism%22">Energy metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22Mice%22">Mice</searchLink><br /><searchLink fieldCode="DE" term="%22Experimental+design%22">Experimental design</searchLink><br /><searchLink fieldCode="DE" term="%22Fibrosis%22">Fibrosis</searchLink><br /><searchLink fieldCode="DE" term="%22Genes%22">Genes</searchLink><br /><searchLink fieldCode="DE" term="%22Metabolites%22">Metabolites</searchLink><br /><searchLink fieldCode="DE" term="%22Pollutants%22">Pollutants</searchLink><br /><searchLink fieldCode="DE" term="%22Animal+experimentation%22">Animal experimentation</searchLink><br /><searchLink fieldCode="DE" term="%22Western+immunoblotting%22">Western immunoblotting</searchLink><br /><searchLink fieldCode="DE" term="%22One-way+analysis+of+variance%22">One-way analysis of variance</searchLink><br /><searchLink fieldCode="DE" term="%22Liver%22">Liver</searchLink><br /><searchLink fieldCode="DE" term="%22Inflammation%22">Inflammation</searchLink>
– Name: SubjectGeographic
  Label: Geographic Terms
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22China%22">China</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: BACKGROUND: Fat-soluble toxicants, such as chlorpyrifos (CPF) can accumulate in adipose tissue and the liver. During weight loss, these compounds may be released into the circulation, but the metabolic consequences of this mobilization remain poorly understood. OBJECTIVES: This study aimed to investigate the mobilization of CPF during weight loss and its effects on liver health and adipose tissue metabolism in mice. METHODS: C57BL/6J mice were fed a high-fat diet (HFD) or a low-fat diet (LFD) and exposed to 2 mg/kg BW/day CPF by oral gavage. Weight loss was induced by β3-adrenergic stimulation (CL316243) or treadmill exercise for 4 or 10 weeks. CPF was quantified in serum and tissues using HPLC. Tissue histology, expression of genes related to CPF metabolism, liver injury markers, and metabolic protein levels were assessed. RESULTS: CPF-exposed LFD mice showed more severe liver fibrosis and adipose inflammation than did their HFD counterparts. While obese mice had lower adipose CPF concentrations, they showed higher hepatic accumulation. CPF-exposed weight loss mice had higher levels of CPF in adipose tissue, liver, and brain and higher expression of CPF metabolism-related genes, including Paraoxinase-1 and cytochrome P450 genes, and greater glucose intolerance compared to their counterparts without CPF administration. Molecular analyses revealed suppressed AMPK signaling and P62 accumulation, indicating mitophagy disruption in CPF-exposed mice after weight loss. These effects occurred even at human-relevant low doses (0.45 mg/kg of BW/day) and persisted across sexes. DISCUSSION: Weight loss mobilizes CPF and its metabolites from fat stores, leading to tissue accumulation and damage. Even low-dose exposure contributes to hepatic and metabolic disruption in mice, highlighting the potential risk of toxicant mobilization during fat reduction. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
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  Data: <i>Copyright of Environmental Health Perspectives is the property of National Institute of Environmental Health Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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      – Type: doi
        Value: 10.1021/EHP.6c00042
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        Text: English
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      – SubjectFull: Weight loss
        Type: general
      – SubjectFull: High performance liquid chromatography
        Type: general
      – SubjectFull: Glucose intolerance
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      – SubjectFull: Adipose tissues
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      – SubjectFull: Reverse transcriptase polymerase chain reaction
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      – SubjectFull: AMP-activated protein kinases
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      – SubjectFull: Liver
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      – SubjectFull: Inflammation
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      – SubjectFull: China
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      – TitleFull: Mobilization of the Environmental Toxicant Chlorpyrifos during Weight Loss and Its Impact on Liver and Adipose Tissue Metabolism in Mice.
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