Permethrin decreased insulin secretion and the expression of proteins linked to metabolism and exocytosis in INS832/3 pancreatic beta cells

IF 4.2 3区环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES

Environmental toxicology and pharmacology Pub Date : 2026-03-01 Epub Date: 2026-01-28 DOI:10.1016/j.etap.2026.104952

Nela Pavlikova, Jan Sramek, Kamila Balusikova, Vlasta Nemcova

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Abstract

Permethrin, a widely used pyrethroid insecticide, has been suspected of contributing to metabolic disturbances, insulin resistance, and diabetes, but its effect on pancreatic beta cells has never been investigated. We evaluated the impact of one-week exposure to sublethal concentrations (1 μM and 10 μM) of permethrin on the function and viability of INS832/3 pancreatic beta cells. Permethrin significantly decreased glucose- and KCl-stimulated insulin secretion despite only a partial reduction in intracellular insulin levels. It also altered the expression of proteins involved in glucose metabolism, energy sensing, lipid storage and exocytosis machinery, suggesting a multifaceted impairment of cell functioning. A comparative analysis using HepG2 liver cells revealed tissue-specific responses. This is the first report showing that permethrin exposure decreases insulin secretion by pancreatic beta cells. This data can help to better evaluate the risk assessment of permethrin as a potential endocrine disruptor that may increase the risk of diabetes.

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氯菊酯降低INS832/3胰腺β细胞胰岛素分泌及代谢和胞吐相关蛋白表达

氯菊酯是一种广泛使用的拟除虫菊酯杀虫剂，被怀疑会导致代谢紊乱、胰岛素抵抗和糖尿病，但其对胰腺细胞的影响从未被研究过。我们评估了暴露于亚致死浓度（1 μM和10 μM）的氯菊酯一周对INS832/3胰腺β细胞功能和活力的影响。氯菊酯显著降低葡萄糖和氯化钾刺激的胰岛素分泌，尽管细胞内胰岛素水平仅部分降低。它还改变了参与葡萄糖代谢、能量感知、脂质储存和胞吐机制的蛋白质的表达，表明细胞功能受到多方面的损害。使用HepG2肝细胞的比较分析揭示了组织特异性反应。这是首次有报告显示，接触氯菊酯会减少胰腺细胞分泌胰岛素。这些数据有助于更好地评估氯菊酯作为可能增加糖尿病风险的潜在内分泌干扰物的风险评估。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Environmental toxicology and pharmacology 医学-毒理学

CiteScore

7.00

自引率

4.70%

发文量

185

审稿时长

34 days

期刊介绍： Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.