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Exploring the Mechanism of Kidney Injury in Mice Induced by High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Through the Kidney-Gut Axis
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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.
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 Mechanismof Kidney Injury in Mice Inducedby High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Throughthe Kidney-Gut Axis
AI summary Read the abstract
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.
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.
Polystyrene microplastics induce kidney injury via gut barrier dysfunction and C5a/C5aR pathway activation
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In a mouse study, polystyrene microplastics caused kidney damage by first breaking down the gut barrier, which then triggered an immune response that attacked the kidneys through a specific pathway called C5a/C5aR. When researchers repaired the gut barrier or blocked this immune pathway, the kidney damage was prevented. This study reveals a gut-kidney connection that could explain how swallowing microplastics might lead to kidney problems in humans.
High-fat diet primes vulnerability to polyethylene terephthalate nanoplastic toxicity via the gut microbiota-metabolism axis
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Mice on a high-fat diet suffered much more gut damage from plastic nanoparticles (the kind found in food packaging) than mice on a normal diet, including a leakier gut lining, more inflammation, and disrupted gut bacteria. This suggests that eating a high-fat diet may make your gut more vulnerable to the harmful effects of the tiny plastic particles we're increasingly exposed to through food and water, meaning diet and plastic exposure together could pose a bigger health risk than either one alone.
Dietary patterns reshape organ-specific biodistribution and toxicity upon exposure to polystyrene nanoplastics: role of ROS-mediated intestinal senescence
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A new mouse study suggests that what you eat may change how nanoplastics (tiny plastic particles from food and packaging) affect your body. Mice on a high-fat diet showed more kidney damage from nanoplastic exposure, while mice on a high-sugar diet showed more liver damage, both linked to plastic-triggered stress that ages and weakens the gut lining. This suggests that poor diet may not just cause health problems on its own, but could also make the body more vulnerable to harm from the microplastics we're increasingly exposed to in daily life.
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