Niu Huixia, Yang Ying, Zhou Yuting, Ma Xue, Ding Zhehao, Xu Manjin, Wu Lizhi, Li Xueqing, Xing Mingluan, Zhang Qin, Chen Hao, Tao Xiongwei, Mo Zhe, Chen Zhijian, Tu Pengcheng, Lou Xiaoming
Center for Disease Control and Prevention of Jinyun County, 89 Cuizhu Road, Jinyun 321400, China.
Zhejiang Provincial Center for Disease Control and Prevention, 3399 Binsheng Road, Hangzhou 310051, China.
Metabolites. 2025 Aug 20;15(8):557. doi: 10.3390/metabo15080557.
Despite escalating global pollution from microplastics (MPs) and the concurrent surge in high-fat food consumption, the health impacts of MP exposure on individuals under different dietary patterns remain poorly understood.
This study investigated the differential effects of environmentally relevant concentrations of polystyrene microplastics (5 μm, 8 mg/kg) on gut barrier function in mice fed either a normal chow diet (CD) or a high-fat diet (HFD).
Key findings revealed that, in HFD-fed mice, MP exposure significantly reduced ( < 0.05) the transcriptional levels of genes encoding the tight junction proteins (ZO-1, Occludin, and Claudin-1), as well as the mucin protein Muc-2, accompanied by decreased protein expression levels of these markers in both colonic and ileal tissues. In contrast, no significant differences were observed in CD-fed mice exposed to MPs. Analysis of the gut microbiota and measurement of short-chain fatty acid (SCFA) metabolites showed that MPs induced significant alterations in the composition and diversity indices of the gut microbiota, along with a marked decrease ( < 0.05) in the levels of the characteristic metabolite butyrate in HFD-fed mice. Conversely, butyrate levels remained unchanged in CD-fed mice following MP exposure. Quantitative PCR (qPCR) and immunofluorescence staining of colonic tissues demonstrated that MP exposure significantly downregulated ( < 0.05) both the transcription and protein expression of peroxisome proliferator-activated receptor γ (PPARγ) in HFD-fed mice. Again, no significant changes were detected in CD-fed mice.
These results collectively indicate that the impact of microplastics on the intestinal barrier differs significantly between mice fed normal and high-fat diets. The gut microbiota and its metabolites, particularly butyrate, may play a critical role, possibly through modulating PPARγ signaling. This study contributes valuable insights into understanding the toxicity profiles of microplastics and establishing crucial links between dietary patterns and the health effects of emerging pollutants.
尽管全球微塑料（MPs）污染不断加剧，同时高脂肪食物的消费量也在激增，但不同饮食模式下MPs暴露对个体健康的影响仍知之甚少。
本研究调查了环境相关浓度的聚苯乙烯微塑料（5μm，8mg/kg）对正常饮食（CD）或高脂饮食（HFD）喂养的小鼠肠道屏障功能的不同影响。
主要研究结果表明，在高脂饮食喂养的小鼠中，MPs暴露显著降低（<0.05）了编码紧密连接蛋白（ZO-1、闭合蛋白和Claudin-1）以及粘蛋白Muc-2的基因的转录水平，同时结肠和回肠组织中这些标志物的蛋白表达水平也降低。相比之下，正常饮食喂养且暴露于MPs的小鼠未观察到显著差异。对肠道微生物群的分析和短链脂肪酸（SCFA）代谢物的测量表明，MPs诱导了肠道微生物群组成和多样性指数的显著改变，同时高脂饮食喂养的小鼠中特征代谢物丁酸盐的水平显著降低（<0.05）。相反，正常饮食喂养的小鼠在MPs暴露后丁酸盐水平保持不变。结肠组织的定量PCR（qPCR）和免疫荧光染色表明，MPs暴露显著下调（<0.05）了高脂饮食喂养小鼠中过氧化物酶体增殖物激活受体γ（PPARγ）的转录和蛋白表达。同样，正常饮食喂养的小鼠未检测到显著变化。
这些结果共同表明，微塑料对正常饮食和高脂饮食喂养的小鼠肠道屏障的影响存在显著差异。肠道微生物群及其代谢物，特别是丁酸盐，可能发挥关键作用，可能是通过调节PPARγ信号传导。本研究为理解微塑料的毒性特征以及建立饮食模式与新兴污染物健康影响之间的关键联系提供了有价值的见解。
