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聚苯乙烯纳米塑料对 2 型糖尿病小鼠模型的作用及其机制评价。

The effect and a mechanistic evaluation of polystyrene nanoplastics on a mouse model of type 2 diabetes.

机构信息

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, 430079, Hubei, China.

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, 430079, Hubei, China.

出版信息

Food Chem Toxicol. 2023 Mar;173:113642. doi: 10.1016/j.fct.2023.113642. Epub 2023 Feb 2.

DOI:10.1016/j.fct.2023.113642
PMID:36736609
Abstract

Nanoplastics have become ubiquitous in the global environment and have attracted increasing attention. However, whether there is an influence between exposure to nanoplastics and diabetes is unclear. To determine the effects of exposure to Polystyrene nanoplastics (PS-NPs) and evaluate the underlying mechanisms, mice were orally exposed to PS-NPs at dosages of 1, 10, 30 mg/kg/day for 8 weeks, alone or combined with a high fat diet and streptozocin (STZ) injection. Our data showed that exposure to 30 mg/kg/day PS-NPs alone induced a significant increase in blood glucose, glucose intolerance and insulin resistance. Combined with a high fat diet and STZ injection, PS-NPs exposure markedly aggravated oxidative stress, glucose intolerance, insulin tolerance and insulin resistance, and induced lesions in the liver and pancreas. PS-NPs exposure could decrease the phosphorylation of AKT and GSK3β, and treatment with SC79, a selective AKT activator, could increase the level of AKT and GSK3β phosphorylation, effectively alleviating the increase in ROS levels in the liver or pancreas, and slightly attenuating the increase in fasting blood glucose levels and insulin resistance induced by PS-NPs exposure. This showed that exposure to PS-NPs aggravated type 2 diabetes and the underlying mechanism partly involved in the inhibition of AKT/GSK3β phosphorylation.

摘要

纳米塑料在全球环境中无处不在,引起了越来越多的关注。然而,暴露于纳米塑料与糖尿病之间是否存在影响尚不清楚。为了确定暴露于聚苯乙烯纳米塑料(PS-NPs)的影响并评估其潜在机制,我们将小鼠以 1、10、30mg/kg/天的剂量经口暴露于 PS-NPs 中,持续 8 周,单独或与高脂肪饮食和链脲佐菌素(STZ)注射联合暴露。我们的数据表明,单独暴露于 30mg/kg/天 PS-NPs 可显著增加血糖、葡萄糖耐量受损和胰岛素抵抗。与高脂肪饮食和 STZ 注射联合暴露时,PS-NPs 暴露明显加重氧化应激、葡萄糖耐量受损、胰岛素耐受和胰岛素抵抗,并导致肝脏和胰腺损伤。PS-NPs 暴露可降低 AKT 和 GSK3β 的磷酸化水平,而选择性 AKT 激活剂 SC79 的处理可增加 AKT 和 GSK3β 磷酸化水平,有效缓解 PS-NPs 暴露引起的肝脏或胰腺中 ROS 水平升高,并轻微减轻 PS-NPs 暴露引起的空腹血糖水平升高和胰岛素抵抗。这表明暴露于 PS-NPs 加重了 2 型糖尿病,其潜在机制部分涉及 AKT/GSK3β 磷酸化的抑制。

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