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Exploring the Mechanismof Kidney Injury in Mice Inducedby High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Throughthe Kidney-Gut Axis
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This mouse study found that combining a high-fat diet with polystyrene nanoplastic exposure (100 nm, 25 mg/kg/day) worsened kidney toxicity beyond high-fat diet alone, with the combination disrupting lipid metabolism via tryptophan and glycerophospholipid pathways and exacerbating gut microbiota dysbiosis through the kidney-gut axis.
This research aimed to establish a murine model of kidney injury induced by a combination of high-fat diet (HFD) and polystyrene nanoplastics (PS-NPs), and explored the underlying mechanisms from the perspective of the kidney-gut axis. Our results indicated that HFD combined with PS-NPs (100 nm, 25 mg/kg/d) exposure exacerbated kidney toxicity compared to HFD, as evidenced by significant increases in kidney injury markers, such as blood urea nitrogen (BUN), creatinine (CRE), kidney injury molecule 1 (KIM-1), cystatin C (Cys-C) (P < 0.05). In addition, the total cholesterol (TC), triglycerides (TG), nonesterified fatty acids (NEFA), interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA) levels were notably increased (P < 0.05), while the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were notably decreased (P < 0.05) after exposure to HFD combined with PS-NPs. Further investigation into the underlying mechanisms revealed that the combination of PS-NPs and HFD disrupts mouse lipid metabolism through pathways involving tryptophan metabolism and glycerophospholipid metabolism, exacerbating the disorder of gut microbiota. Our research demonstrates for the first time that exposure to PS-NPs exacerbates metabolic disorders and renal toxicity in mice fed an HFD via the kidney-gut axis.
More Papers Like This
Exploring the Mechanism of Kidney Injury in Mice Induced by High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Through the Kidney-Gut Axis
AI summary Read the abstract
In a mouse study, the combination of a high-fat diet and polystyrene nanoplastics caused worse kidney damage than either exposure alone, working through the kidney-gut connection. The nanoplastics plus high-fat diet disrupted gut bacteria, increased inflammation, and triggered a harmful immune response that traveled from the gut to the kidneys. This suggests that people who eat high-fat diets may be more vulnerable to kidney damage from nanoplastic exposure.
Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
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Researchers co-exposed rats to polystyrene nanoplastics and the antibiotic gentamicin and found that the combination caused significantly greater kidney damage than either substance alone, amplifying oxidative stress, inflammation, and mitochondrial apoptosis in a synergistic manner.
Single-cell RNA-seq analysis decodes the kidney microenvironment induced by polystyrene microplastics in mice receiving a high-fat diet
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Using advanced single-cell gene analysis, researchers found that mice fed both polystyrene microplastics and a high-fat diet suffered significantly worse kidney damage than either exposure alone. The combination reshaped the kidney's cellular environment, promoting scarring, triggering cancer-related pathways, and altering immune cell populations. This is particularly relevant to human health because many people are simultaneously exposed to microplastics through food and drink while also consuming high-fat diets.
Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys
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Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.
Long-Term Exposure to Polystyrene Microspheres and High-Fat Diet-Induced Obesity in Mice: Evaluating a Role for Microbiota Dysbiosis.
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A long-term mouse study examined how chronic exposure to polystyrene microspheres interacts with a high-fat diet to affect obesity-related outcomes, finding that microplastics worsened metabolic disruption and fat accumulation compared to diet alone. The results raise concern that microplastic exposure may be an environmental factor contributing to the global obesity epidemic.
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