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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.
This study investigated whether a high-fat diet (HFD) acts as a priming factor that increases intestinal susceptibility to polyethylene terephthalate nanoplastics (PET-NPs, 100 nm, 25 mg/kg/d). After a 12-week combined exposure in mice, HFD priming potentiated the deleterious effects of PET-NPs on intestinal structure and function. Compared to HFD alone, the combined exposure (HFD + PET-NPs) exacerbated intestinal barrier injury, as evidenced by reduced tight junction proteins (Claudin-1, Occludin, and ZO-1), increased permeability, and disrupted histoarchitecture. These mice also exhibited enhanced oxidative stress, elevated inflammation (IL-1β, IL-6, and TNF-α), and exacerbated gut microbiota dysbiosis, characterized by a Firmicutes-dominated structure with decreased Lactobacillus and increased pro-inflammatory genera (Faecalibaculum, Lachnoclostridium, Romboutsia, and norank_f__Desulfovibrionaceae). Metabolomic analysis identified glycerophospholipid metabolism as the primary perturbed pathway, with additional alterations in sphingolipid, galactose, pentose phosphate, and tryptophan metabolism. Together, these findings suggest that HFD primes the gut for enhanced PET-NPs induced injury through microbiota-metabolism interactions, offering correlative insights into combined dietary-environmental health risks.
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Researchers found that polystyrene microplastics caused metabolic problems like diabetes and fatty liver disease in mice, but only when combined with a high-fat diet. The high-fat diet appeared to damage the gut lining enough to allow microplastics to deposit in the intestinal wall, triggering inflammation that altered nutrient absorption. This suggests that people with poor diets may be more vulnerable to the harmful effects of microplastic exposure.
Oral exposure to polyethylene microplastics of adult male mice fed a normal or western-style diet: impact on gut and gut-liver axis homeostasis
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Researchers orally exposed adult male mice to polyethylene microplastics under both normal and high-fat diets, assessing effects on the gastrointestinal tract. The study found that diet influences microplastic-induced gut changes, with greater effects observed in animals fed a western-style high-fat diet.
Effects of frying on microplastics load in fish and implications on health
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Researchers investigated the effects of polyethylene microplastics on gut microbiota composition in mice fed a high-fat diet, finding that microplastic exposure altered microbial diversity and increased gut permeability. Co-exposure with a high-fat diet amplified metabolic disruption.
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.
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