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

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

  • Environ Res. 2025 Oct 21:287:123171. doi: 10.1016/j.envres.2025.123171.
Zhongyuan Zhang 1,  Jiaming Fu 1,  Yihong Di 1,  Honghui Li 1,  Bing Wu 1,  Xueyan Tian 1,  Meiyan Li 1,  Yuqing Dai 1,  Zhuoheng Shen 1,  Jinhao Jia 1,  Zeyang Bai 1,  Limeng Xiong 1,  Yuhan Zhang 1,  Xiaoyu Li 1,  Yi Zhao 1,  Hao Hu 2,  Guangjun Wang 2,  Huifang Yang 3,  Rui Zhang 4,  Jian Sun 5
Affiliations

Affiliations

  • 1 School of Public Health, Department of Medical Records and Statistics, General Hospital of Ningxia Medical University, Ningxia Medical University, Yinchuan, Ningxia, 750004, PR China; Ningxia Key Laboratory of Environmental Factors and Chronic Disease Control, Yinchuan, 750004, Ningxia, PR China.
  • 2 Yinchuan Center for Disease Control and Prevention, Yinchuan, Ningxia, 750004, PR China.
  • 3 School of Public Health, Department of Medical Records and Statistics, General Hospital of Ningxia Medical University, Ningxia Medical University, Yinchuan, Ningxia, 750004, PR China; Ningxia Key Laboratory of Environmental Factors and Chronic Disease Control, Yinchuan, 750004, Ningxia, PR China. Electronic address: joyceyhf@163.com.
  • 4 School of Public Health, Department of Medical Records and Statistics, General Hospital of Ningxia Medical University, Ningxia Medical University, Yinchuan, Ningxia, 750004, PR China; Ningxia Key Laboratory of Cerebrocranial Disease, Incubation Base of National Key Laboratory, Yinchuan, 750004, Ningxia, PR China. Electronic address: z_zhangrui@163.com.
  • 5 School of Public Health, Department of Medical Records and Statistics, General Hospital of Ningxia Medical University, Ningxia Medical University, Yinchuan, Ningxia, 750004, PR China; Ningxia Key Laboratory of Environmental Factors and Chronic Disease Control, Yinchuan, 750004, Ningxia, PR China. Electronic address: 20180016@nxmu.edu.cn.
PMID: 41130505 DOI: 10.1016/j.envres.2025.123171
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.

Keywords

Diabetes; Imidacloprid; MIN6 cells; Mitochondrial apoptosis; NF-κB; Pancreatic β-cells.

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