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Oral exposure to nanoplastics altered lipid profiles in mouse intestine
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Researchers exposed mice to nanoplastics orally for 14 days and found significant changes in lipid profiles within their intestinal tissue, even without visible tissue damage. The nanoplastics disrupted key fat metabolism pathways and triggered signs of abnormal cellular cleanup processes called autophagy. The study suggests that nanoplastic ingestion may alter how the gut processes fats, with potential implications for metabolic health.
The wide uses of plastics lead to nanoplastic exposure in reality. Previous studies reported that micro- and nano-plastics (MNPs) disrupted metabolism, but few studies investigated lipid profile changes. Hereby, we exposed mice to vehicles (control), 0.05 or 0.5 mg/kg 20 or 100 nm nanoplastics via gavage, once a day, for 14 days. Albeit no obvious tissue damage, lipidomics data revealed 76 up-regulated and 29 down-regulated lipid molecules in mouse intestines. Further analysis revealed that a number of up-regulated lipid molecules belong to glycerophospholipid (GP). Among GP, we noticed an up-regulation of 9 phosphatidylserine (PS) molecules, and we further verified the presence of autophagosomes and co-localization of typical autophagic lipolysis proteins in intestinal sections, as well as decreased lysosomal associated protein 2 (LAMP2) and increased adipose triglyceride lipase (ATGL) in intestinal homogenates, indicating perturbed autophagic pathway. The exposure also up-regulated 9 phosphatidylinositol (PI) molecules, and we verified a significant decrease of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), indicating altered PI3K-signaling pathway. Besides GP, nanoplastics also significantly up-regulated some sphingolipids (SP), such as ceramide (Cer), and some sterol lipids, such as cholesterol derivatives. Combined, these results suggested that oral exposure to nanoplastics altered lipid profiles and related signaling pathway in mouse intestines.
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Mice were exposed to polyethylene terephthalate nanoparticles, and researchers used histopathology, metabolomics, and metagenomics to track downstream effects. Nanoplastic ingestion caused severe metabolic disruption—including weight loss, organ atrophy, and liver-intestinal dysfunction—by remodeling the bile acid–gut microbiota axis.
Interactions between intestinal microbiota and metabolites in zebrafish larvae exposed to polystyrene nanoplastics: Implications for intestinal health and glycolipid metabolism
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Zebrafish larvae exposed to polystyrene nanoplastics suffered intestinal damage, including inflammation, oxidative stress, and disrupted gut bacteria -- with increases in bacteria linked to gut disease. The nanoplastics also altered metabolism related to sugar and fat processing, suggesting that ingesting these tiny particles could harm digestive health and disrupt how the body processes nutrients.
Lipidomics Approaches Reveal Tissue-Specific Lipidome Remodeling Induced by Micro- and Nanoplastic Exposure
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This review pulls together animal research showing that tiny plastic particles (microplastics and nanoplastics) don't just cause general irritation in the body — they specifically mess with fats in our cells, disrupting cell membranes and energy production in organs like the liver, kidneys, lungs, and brain. This matters because fat molecules help cells function properly, and this early damage could set the stage for bigger health problems like liver disease, metabolic issues, or brain-related harm, though more research is needed to confirm how this plays out in humans.
Long-Term Exposure to Environmentally Relevant Doses of Large Polystyrene Microplastics Disturbs Lipid Homeostasis via Bowel Function Interference
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Researchers exposed mice to environmentally relevant doses of large polystyrene microplastics in their diet for 21 weeks and found significant disruptions to fat metabolism and gut bacterial communities. The microplastics interfered with bowel function, which in turn altered how the body processes and stores lipids. The study provides evidence that even low-level, long-term microplastic exposure through food may affect metabolic health in mammals.
Continuous oral exposure to micro- and nanoplastics induced gut microbiota dysbiosis, intestinal barrier and immune dysfunction in adult mice
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Researchers fed mice micro- and nanoplastics at environmentally relevant levels and found significant gut damage, including disrupted gut bacteria, weakened intestinal barriers, and reduced immune function. The ratio of beneficial to harmful gut bacteria shifted, and immune cells in the gut decreased. Importantly, the duration of exposure and the size of plastic particles mattered more than the amount consumed, suggesting even low-level long-term exposure could harm gut health.
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