Increasing attention is being paid to the environmental and health impacts of nanoplastics (NPs) pollution. Exposure to nanoplastics (NPs) with different charges and functional groups may have different adverse effects after ingestion by organisms, yet the potential ramifications on mammalian blood glucose levels, and the risk of diabetes remain unexplored. Mice were exposed to PS-NPs/COOH/NH2 at a dose of 5 mg/kg/day for nine weeks, either alone or in a T2DM model. The findings demonstrated that exposure to PS-NPs modified by different functional groups caused a notable rise in fasting blood glucose (FBG) levels, glucose intolerance, and insulin resistance in a mouse model of T2DM. Exposure to PS-NPs-NH2 alone can also lead the above effects to a certain degree. PS-NPs exposure could induce glycogen accumulation and hepatocellular edema, as well as injury to the pancreas. Comparing the effect of different functional groups or charges on T2DM, the PS-NPs-NH2 group exhibited the most significant FBG elevation, glycogen accumulation, and insulin resistance. The phosphorylation of AKT and FoxO1 was found to be inhibited by PS-NPs exposure. Treatment with SC79, the selective AKT activator was shown to effectively rescue this process and attenuate T2DM like lesions. Exposure to PS-NPs with different functional groups (charges) induced T2DM-like lesions. Amino-modified PS-NPs cause more serious T2DM-like lesions than pristine PS-NPs or carboxyl functionalized PS-NPs. The underlying mechanisms involved the inhibition of P-AKT/P-FoxO1. This study highlights the potential risk of NPs pollution on T2DM, and provides a new perspective for evaluating the impact of plastics aging.

中文翻译：

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不同官能团和电荷的聚苯乙烯纳米塑料对2型糖尿病的影响不同


人们越来越关注纳米塑料（NP）污染对环境和健康的影响。接触具有不同电荷和官能团的纳米塑料（NP）在被生物体摄入后可能会产生不同的不良影响，但其对哺乳动物血糖水平和糖尿病风险的潜在影响仍未被探索。小鼠单独或在 T2DM 模型中以 5 mg/kg/天的剂量暴露于 PS-NPs/COOH/NH2 九周。研究结果表明，暴露于不同功能基团修饰的 PS-NP 会导致 T2DM 小鼠模型的空腹血糖 (FBG) 水平、葡萄糖耐受不良和胰岛素抵抗显着升高。单独接触PS-NPs-NH2也会在一定程度上导致上述效应。 PS-NPs 暴露可能引起糖原积累和肝细胞水肿，以及胰腺损伤。比较不同功能组或电荷对 T2DM 的影响，PS-NPs-NH2 组表现出最显着的 FBG 升高、糖原积累和胰岛素抵抗。发现 PS-NP 暴露会抑制 AKT 和 FoxO1 的磷酸化。 SC79（选择性 AKT 激活剂）治疗被证明可以有效挽救这一过程并减轻 T2DM 样病变。暴露于具有不同官能团（电荷）的 PS-NP 会诱导 T2DM 样病变。氨基修饰的 PS-NP 比原始 PS-NP 或羧基功能化的 PS-NP 引起更严重的 T2DM 样病变。潜在机制涉及 P-AKT/P-FoxO1 的抑制。该研究强调了NPs污染对T2DM的潜在风险，并为评估塑料老化的影响提供了新的视角。