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Imidacloprid induces abnormal glucose metabolism through NF-κB-mediated apoptosis of pancreatic β cells based on population exposure levels.

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Title: Imidacloprid induces abnormal glucose metabolism through NF-κB-mediated apoptosis of pancreatic β cells based on population exposure levels.
Authors: Zhang, Zhongyuan1,2 (AUTHOR), Fu, Jiaming1,2 (AUTHOR), Di, Yihong1,2 (AUTHOR), Li, Honghui1,2 (AUTHOR), Wu, Bing1,2 (AUTHOR), Tian, Xueyan1,2 (AUTHOR), Li, Meiyan1,2 (AUTHOR), Dai, Yuqing1,2 (AUTHOR), Shen, Zhuoheng1,2 (AUTHOR), Jia, Jinhao1,2 (AUTHOR), Bai, Zeyang1,2 (AUTHOR), Xiong, Limeng1,2 (AUTHOR), Zhang, Yuhan1,2 (AUTHOR), Li, Xiaoyu1,2 (AUTHOR), Zhao, Yi1,2 (AUTHOR), Hu, Hao3 (AUTHOR), Wang, Guangjun3 (AUTHOR), Yang, Huifang1,2 (AUTHOR) joyceyhf@163.com, Zhang, Rui1,4 (AUTHOR) z_zhangrui@163.com, Sun, Jian1,2 (AUTHOR) 20180016@nxmu.edu.cn
Source: Environmental Research. Dec2025, Vol. 287, pN.PAG-N.PAG. 1p.
Subjects: Imidacloprid, Glucose metabolism, NF-kappa B, Environmental exposure, Diabetes, Apoptosis, Toxicology, Pancreatic beta cells
Abstract: Previous epidemiologic studies have indicated a positive association between population-based imidacloprid (IMI) exposure and diabetes. Moreover, toxicological evidence suggests that IMI can disrupt glucose metabolism in non-target organisms. However, the toxic doses of IMI in previous experimental studies were much higher than the exposure levels in the real world, and the underlying mechanism remains unknown. In this study, based on the exposure level of neonicotinoids in humans, we investigated the possible mechanism of IMI-induced glucose metabolism disorders using cybertoxicology predictions, a long-term exposure model of IMI in mice, and cellular models. The cybertoxicology predictions showed that NF-κB and apoptosis play key roles in the association of IMI, pancreatic β-cell injury, and diabetes. However, exposure of mice to IMI through potable water (104 μg/kg, population exposure maximum) for 24 weeks did not result in abnormal glucose metabolism (P > 0.05), while significant activation of inflammatory response, NF-κB phosphorylation, and mitochondrial apoptosis pathways were observed (P < 0.05). After inhibition of NF-κB P65 phosphorylation in the cellular model, IMI-induced alterations in the MIN6 cell structure and function, inflammatory responses, and mitochondrial apoptotic pathways were alleviated (P < 0.05). This finding provides evidence for the disruption of glucose metabolism due to long-term exposure to IMI, and subsequent studies should focus on the effects of longer exposure to IMI on glucose metabolism as well as the role of the NF-κB signaling pathway. [Display omitted] • Cybertoxicology predicted NF-κB and apoptosis as key targets for IMI-induced diabetes. • Population-based IMI exposure in mice activated pancreatic NF-κB and mitochondrial apoptosis. • NF-κB inhibition alleviated IMI-induced β-cell dysfunction and apoptosis in vitro. [ABSTRACT FROM AUTHOR]
Copyright of Environmental Research is the property of Academic Press Inc. 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: Imidacloprid induces abnormal glucose metabolism through NF-κB-mediated apoptosis of pancreatic β cells based on population exposure levels.
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  Data: &lt;searchLink fieldCode=&quot;JN&quot; term=&quot;%22Environmental+Research%22&quot;&gt;Environmental Research&lt;/searchLink&gt;. Dec2025, Vol. 287, pN.PAG-N.PAG. 1p.
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  Data: Previous epidemiologic studies have indicated a positive association between population-based imidacloprid (IMI) exposure and diabetes. Moreover, toxicological evidence suggests that IMI can disrupt glucose metabolism in non-target organisms. However, the toxic doses of IMI in previous experimental studies were much higher than the exposure levels in the real world, and the underlying mechanism remains unknown. In this study, based on the exposure level of neonicotinoids in humans, we investigated the possible mechanism of IMI-induced glucose metabolism disorders using cybertoxicology predictions, a long-term exposure model of IMI in mice, and cellular models. The cybertoxicology predictions showed that NF-κB and apoptosis play key roles in the association of IMI, pancreatic β-cell injury, and diabetes. However, exposure of mice to IMI through potable water (104 μg/kg, population exposure maximum) for 24 weeks did not result in abnormal glucose metabolism (P &gt; 0.05), while significant activation of inflammatory response, NF-κB phosphorylation, and mitochondrial apoptosis pathways were observed (P &lt; 0.05). After inhibition of NF-κB P65 phosphorylation in the cellular model, IMI-induced alterations in the MIN6 cell structure and function, inflammatory responses, and mitochondrial apoptotic pathways were alleviated (P &lt; 0.05). This finding provides evidence for the disruption of glucose metabolism due to long-term exposure to IMI, and subsequent studies should focus on the effects of longer exposure to IMI on glucose metabolism as well as the role of the NF-κB signaling pathway. [Display omitted] • Cybertoxicology predicted NF-κB and apoptosis as key targets for IMI-induced diabetes. • Population-based IMI exposure in mice activated pancreatic NF-κB and mitochondrial apoptosis. • NF-κB inhibition alleviated IMI-induced β-cell dysfunction and apoptosis in vitro. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: &lt;i&gt;Copyright of Environmental Research is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites without the copyright holder&#39;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.&lt;/i&gt; (Copyright applies to all Abstracts.)
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        Value: 10.1016/j.envres.2025.123171
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        Text: English
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      – SubjectFull: Pancreatic beta cells
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