0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Human Health Effects Reproductive & Development Sign in to save

Polystyrene microplastics disturb maternal glucose homeostasis and induce adverse pregnancy outcomes

Ecotoxicology and Environmental Safety 2024 28 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Ruiying Zhang, Yueying Feng, Penghui Nie, Wanzhen Wang, Hua Wu, Hua Wu, Xianxian Wan, Hengyi Xu, Fen Fu

Summary

Pregnant mice exposed to polystyrene microplastics developed abnormal blood sugar levels and experienced poor pregnancy outcomes, including placental damage and restricted fetal growth. The study found that microplastics disrupted glucose metabolism through inflammation and a cellular stress response, suggesting that microplastic exposure during pregnancy could contribute to complications similar to gestational diabetes.

Pregnant women are a special group that is sensitive to adverse external stimuli, causing metabolic abnormalities and adverse pregnancy outcomes. Microplastics (MPs), an environmental pollutant widely used in various fields, can induce a variety of toxic responses in mammals. Recent studies verified an association between MPs and metabolic disorders. Our research built a gestational mouse model in which polystyrene microplastics (PS-MPs) of 1 μm size were consumed at concentrations of 0.1, 1, and 10 mg/L during pregnancy. Results indicated that PS-MPs induced placental malfunction and fetal growth retardation. Significant glucose disorders, decreased liver function, hepatic inflammation, and oxidative stress were also observed after PS-MPs exposure. The hepatic SIRT1/IRS1/PI3K pathway was inhibited in the 10 mg/L PS-MPs exposure group. Our study found that PS-MPs activated inflammatory response and oxidative stress by increasing hepatic lipopolysaccharide (LPS) that inhibited the hepatic SIRT1/IRS1/PI3K pathway, ultimately leading to insulin resistance, glucose metabolism disorders, and adverse pregnancy outcomes. This study provides a basis for preventing environment-related gestational diabetes and concomitant adverse pregnancy outcomes.

Share this paper