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61,005 resultsShowing papers similar to Spatial Lipid MetabolicRemodeling from Placenta toMultiple Suborgans during the Gestational Micro- or Nanoplastics Exposure
ClearSpatial Lipid Metabolic Remodeling from Placenta to Multiple Suborgans during the Gestational Micro- or Nanoplastics Exposure
Using pregnant mice exposed to polystyrene micro- and nanoplastics from gestation day 1–18, researchers used MALDI mass spectrometry imaging to construct a comprehensive spatial map of lipid metabolism changes across placenta and multiple maternal and fetal organs, revealing widespread lipid metabolic remodeling.
Polystyrene nanoplastics-induced altered glycolipid metabolism in the liver: A comparative study between pregnant and non-pregnant mice
Researchers compared glycolipid metabolism effects of polystyrene nanoplastics in pregnant versus non-pregnant mice, finding that pregnancy amplified hepatic lipid disruption, with both low and high doses impairing fat metabolism and altering glucose regulation more severely during gestation.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study examined how polypropylene microplastics accumulate in and damage the mouse liver, using integrated lipidomics and transcriptomics to map the molecular landscape of microplastic-induced lipid disruption and metabolic dysfunction.
Maternal exposure to polypropylene nanoplastics disrupts sex- and region-specific lipid metabolism in the brains of C57BL/6N mouse offspring
Pregnant mice were exposed to polypropylene nanoplastics, and offspring brains were analyzed using targeted lipidomics across different brain regions and sexes. The study found that prenatal exposure disrupted lipid metabolism in a sex- and region-specific manner, indicating that early developmental exposure to nanoplastics can have lasting effects on brain biochemistry.
Tissue Distribution of Polystyrene or Mixed Polymer Microspheres and Metabolomic Analysis after Oral Exposure in Mice.
Mice orally exposed to polystyrene or mixed polymer microspheres showed plastic particle distribution across multiple tissues including the liver, kidney, and spleen, with metabolomic analysis revealing distinct alterations in lipid, amino acid, and energy metabolism pathways.
Maternal exposure to polystyrene microplastics alters placental metabolism in mice
Researchers exposed pregnant mice to polystyrene microplastics and examined how placental metabolism was affected. The study found significant changes in placental metabolic pathways that could help explain the fetal growth restriction previously observed in microplastic-exposed pregnancies. These findings suggest that microplastic exposure during pregnancy may interfere with the placenta's ability to support normal fetal development.
Maternal polystyrene nanoplastics exposure during pregnancy induces obesity development in adult offspring through disrupting lipid homeostasis
Researchers found that maternal inhalation exposure to polystyrene nanoplastics during pregnancy induced obesity development in adult offspring of mice, suggesting in utero exposure to airborne nanoplastics programs metabolic dysfunction. The study linked prenatal nanoplastic exposure to increased adiposity and metabolic changes persisting into adulthood.
[The effect and mechanism of exposure to polystyrene nanoplastics on lipid metabolism in mice liver].
Researchers exposed mice to 20 nm polystyrene nanoplastics and investigated the effects on hepatic lipid metabolism using multi-omics approaches. Nanoplastic exposure disrupted lipid metabolic pathways in the liver, causing significant changes in lipid accumulation and related gene expression, suggesting a mechanism by which nanoplastic ingestion may contribute to metabolic disorders.
Molecular Landscape Remodeling Unravels the Cross-Links of Microplastics-Induced Lipidomic Fluctuations, Nutrient Disorders and Energy Disarrangements
Researchers fed mice polypropylene microplastics chronically and used lipidomics and transcriptomics to show that microplastics accumulated in the liver and disrupted lipid metabolism, cholesterol homeostasis, and redox balance, with high doses causing fibrotic liver changes.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers used combined lipidomic and transcriptomic analysis to demonstrate that polypropylene microplastics accumulated in mouse liver and disrupted key metabolic pathways including lipid biosynthesis, cholesterol metabolism, and energy homeostasis.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers examined polypropylene microplastic retention in mouse liver using lipidomics and transcriptomics, finding that chronic exposure disrupted lipid metabolism, cholesterol turnover, and antioxidant defense, with high-dose treatment causing regional liver fibrosis.
Maternal nanoplastic ingestion induces an increase in offspring body weight through altered lipid species and microbiota
Researchers found that when mother mice ingested nanoplastics derived from polystyrene and polypropylene during pregnancy and nursing, their offspring showed increased body weight gain. The weight changes were associated with alterations in fat metabolism and shifts in gut microbiome composition in the pups. The study suggests that maternal exposure to nanoplastic pollution may act as an environmental factor contributing to weight gain in offspring.
Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
Mice exposed to polystyrene nanoplastics for 12 weeks gained weight without eating more and showed increased cholesterol levels and fat accumulation in their livers. Gene and metabolite analysis revealed that the nanoplastics disrupted fat metabolism pathways in the liver, essentially reprogramming how the body processes and stores fat. These findings suggest that nanoplastic exposure could be a hidden factor contributing to obesity and fatty liver disease in humans.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study assessed the liver toxicity of polypropylene microplastics in mice using combined lipidomics and transcriptomics, identifying disrupted lipid metabolism, altered cholesterol handling, and fibrotic tissue remodeling as key pathological outcomes.
Maternal exposure to polystyrene nanoparticles retarded fetal growth and triggered metabolic disorders of placenta and fetus in mice
Researchers exposed pregnant mice to polystyrene nanoplastics through drinking water and found that higher concentrations led to significantly reduced fetal weight. The nanoplastics caused abnormal cell structures in the placenta and disrupted metabolic processes in both placental tissue and fetal livers. The study suggests that maternal nanoplastic exposure during pregnancy can cross the placental barrier and interfere with normal fetal growth and metabolism.
Microplastics and Metabolism: Physiological Responses in Mice Following Ingestion
Researchers found that mice orally exposed to microplastic microspheres showed changes in lipid metabolism and other metabolic pathways, with particles detected in tissues throughout the body. The effects were more pronounced when mice were exposed to mixed microplastic types compared to polystyrene alone, suggesting that real-world mixtures of microplastics may have broader physiological impacts.
Maternal Polystyrene Microplastic Exposure during Gestation and Lactation Altered Metabolic Homeostasis in the Dams and Their F1 and F2 Offspring
Researchers exposed pregnant mice to polystyrene microplastics during pregnancy and nursing and found significant metabolic disruptions in both the mothers and their offspring across two generations. The microplastics altered lipid metabolism, gut microbiota composition, and key metabolic signaling pathways. The study suggests that microplastic exposure during critical developmental windows may have lasting health consequences that pass to future generations.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Mouse liver studies with polypropylene microplastics revealed interconnected disruptions in lipid metabolism, nutrient processing, and energy balance, with proteomic and transcriptomic data highlighting the complexity of hepatic responses to chronic microplastic exposure.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Proteomic and lipidomic profiling of mouse livers after polypropylene microplastic exposure revealed crosstalk between hepatic lipid fluctuations, nutrient metabolism disorders, and energy pathway disarrangements, providing mechanistic insight into microplastic-induced liver toxicity.
Integrated transcriptomics and metabolomics reveal the mechanism of polystyrene nanoplastics toxicity to mice
Researchers used gene expression and metabolic profiling to understand how polystyrene nanoplastics harm mice at the molecular level, finding disrupted energy metabolism, fat processing, and amino acid pathways in the liver. These molecular changes suggest that nanoplastic exposure could contribute to metabolic disorders, with effects becoming more severe at higher doses.
Tissue accumulation of microplastics in mice and biomarker responses suggest widespread health risks of exposure
Researchers fed mice polystyrene microplastics of two sizes and tracked where the particles accumulated in the body, finding them in the liver, kidneys, and gut with distribution patterns depending on particle size. Biochemical analysis revealed that microplastic exposure disrupted energy and fat metabolism, caused oxidative stress, and altered markers of neurotoxicity in the blood. The study provides evidence that microplastics can accumulate in mammalian tissues and may pose widespread health risks.
Dual impact of microplastic exposure in a mouse model: Impaired uterine receptivity and altered maternal-offspring metabolism
Researchers exposed female mice to polystyrene microplastics and found that the particles impaired uterine receptivity, which is critical for embryo implantation, and altered metabolic profiles in both the mothers and their offspring. The microplastics disrupted gene expression related to uterine function and caused metabolic changes across multiple organs. The findings suggest that microplastic exposure could have reproductive and metabolic consequences that extend to the next generation.
Lipidomics and transcriptomics insight into impacts of microplastics exposure on hepatic lipid metabolism in mice
Researchers used lipidomics and transcriptomics to examine how polystyrene microplastic exposure affects liver lipid metabolism in mice over eight weeks. The study found that while body weight and serum lipid levels were not significantly affected, microplastics caused impaired glucose metabolism and specific changes in hepatic lipid profiles, revealing subtle but measurable disruptions to liver function.
Gestational exposure to polystyrene microplastics incurred placental damage in mice: Insights into metabolic and gene expression disorders
This mouse study found that when pregnant mice were exposed to tiny polystyrene microplastics (0.1 micrometers), the particles crossed the placenta and reached fetal livers and brains, causing placental damage and impaired fetal development. Larger microplastics (5 micrometers) were less able to cross the placenta, suggesting that the smallest plastic particles pose the greatest risk during pregnancy.