We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Supporting information.
Summary
Researchers found that nine weeks of oral polystyrene microplastic administration disrupted hepatic lipid, glucose, and amino acid metabolism in leptin-knockout obese mice while also altering fecal microbiota composition, suggesting that microplastic exposure compounds metabolic dysfunction in obesity.
The oral administration of microplastics (MP) for 9 weeks induced disruption of hepatic lipid, glucose, and amino acid metabolism in C57BL/6-Lepem1hwl/Korl (Lep KO) mice with obesity. Therefore, we investigated whether MP-caused hepatic metabolism abnormalities can affect the structural variation of the fecal microbiota during obesity. The overall microbiota profile was analyzed in the feces of Lep KO mice treated with MP for 9 weeks. The lipid accumulation and steatosis area were significantly decreased in MP-treated Lep KO mice. Total microbiota with MP-caused difference identified from feces of Lep KO and wild type (WT) mice were classified into 10 phyla and 106 genera. Among them, two microbial phyla were significantly changed in Lep KO mice after treatment of MP, while significant alterations on 12 genera were detected in Lep KO mice treated with MP. Also, the Chao1 index for richness were remarkably decreased in both MP-treated Lep KO and WT mice, but Shannon index for evenness were increased in only MP-treated Lep KO mice. Therefore, the results of the present study suggest that MP-caused hepatic metabolism disruption may be closely linked to the dysbiosis of the fecal microbiota in Lep KO mice.
Sign in to start a discussion.
More Papers Like This
Disruption of hepatic metabolism in Lep KO mice.
Researchers found that polystyrene microplastics administered orally for nine weeks accumulated in liver tissue of leptin-knockout obese mice and induced histopathological liver alterations, including disruption of hepatic lipid, glucose, and amino acid metabolism.
Dysbiosis of gut microbiota in C57BL/6-Lepem1hwl/Korl mice during microplastics-caused hepatic metabolism disruption
Researchers administered polypropylene microplastics orally to obese mice for 9 weeks and found disruption of hepatic lipid, glucose, and amino acid metabolism alongside structural changes in gut microbiota, with microplastic-treated mice showing decreased hepatic lipid accumulation and altered abundance of specific bacterial genera.
Impact of the Oral Administration of Polystyrene Microplastics on Hepatic Lipid, Glucose, and Amino Acid Metabolism in C57BL/6Korl and C57BL/6-Lepem1hwl/Korl Mice
Researchers investigated the effects of orally administered polystyrene microplastics on liver metabolism in normal and obese mice over eight weeks. They found that microplastic exposure altered lipid, glucose, and amino acid metabolism pathways in the liver and adipose tissues. The study suggests that microplastic ingestion may disrupt hepatic metabolic functions, with potentially different impacts depending on baseline metabolic health status.
Polystyrene microplastics induce gut microbiota dysbiosis and hepatic lipid metabolism disorder in mice
Researchers fed mice two sizes of polystyrene microplastics for five weeks and observed significant disruption of gut bacteria and changes in liver fat metabolism. The microplastics decreased mucus production in the gut and shifted the balance of key bacterial populations at multiple taxonomic levels. The study suggests that microplastic ingestion can trigger gut microbiota imbalance in mammals, which may in turn affect metabolic health.
Long-term exposure to polystyrene microplastics promotes HFD-induced obesity in mice through exacerbating microbiota dysbiosis
Researchers found that long-term polystyrene microplastic exposure worsened high-fat-diet-induced obesity in mice by exacerbating gut microbiota dysbiosis, suggesting microplastic ingestion may amplify metabolic disease risk through disruption of the gut microbiome.