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Maternal polystyrene nanoplastics exposure during pregnancy induces obesity development in adult offspring through disrupting lipid homeostasis
Summary
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.
Abstract Background: Airborne nanoplastics have raised increasing concerns since they become an integral part of daily human activities and pose a potential hazard to health. Previous studies indicated that in utero exposure to environmental toxicants is associated with metabolic dysfunction in later life. However, maternal exposure to polystyrene nanoplastics (PSNPs) during pregnancy through inhalation route on the development of obesity in offspring still unclear. Results: Pregnant dams were exposed to 0 µg/µL (0 particles), 0.5 µg/µL (approximately 0.15 × 1011 particles per day) and 1.0 µg/µL (approximately 0.30 × 1011 particles per day) PSNPs during conception period through oropharyngeal aspiration three times per week. Offspring were sacrificed at postnatal 12 weeks and adipose tissue including perigonadal white adipose tissue and interscapular brown adipose tissue were collected for weight measurement, histopathological observation as well as molecular detection. Our data illustrated that maternal PSNPs exposure during pregnancy induced a decline in birth weight in 0.5 μg/μl but increase postnatal body weight both in 0.5 and 1.0 μg/μl without sex specific manner. Moreover, maternal PSNPs exposure significantly increased the weight of perigonadal white adipose tissue with elevated energy efficiency but not food intake. Furthermore, the genes involved in de novo lipogenesis and uptake of fatty acid in perigonadal white adipose tissue were upregulated after maternal PSNPs exposure; while the gene related with triacylglycerol (TAG) synthesis was simultaneously significantly increased after maternal PSNPs exposure; In addition, maternal PSNPs exposure also upregulated the gene participated in fatty acid oxidation and adipogenesis in female and male offspring. In term of brown adipose tissue, the weight of interscapular brown adipose tissue was increased with upregulated UCP-1expression after maternal PSNPs exposure. Conclusion: In summary, these finding demonstrated that maternal exposure to PSNPs in pregnancy can cause the development of obesity in offspring, which is mainly through the increased genes involved in de novo lipogenesis and uptake of fatty acid as well as genes participated TAG synthesis in perigonadal white adipose tissue.
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