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Polystyrene microplastics impair brown and beige adipocyte function via the gut microbiota-adipose tissue crosstalk in high-fat diet mice
Summary
This mouse study found that polystyrene microplastics impaired the function of brown and beige fat cells, which are important for burning calories and maintaining a healthy metabolism. The microplastics disrupted gut bacteria, which in turn affected how the body regulates fat-burning tissue through the gut-fat tissue connection. These findings suggest that microplastic exposure could contribute to obesity and metabolic problems by undermining the body's natural calorie-burning mechanisms.
BACKGROUND: Microplastics (MPs) are pervasive in the environment and food. The potential health hazards of this emerging pollutant have raised significant concerns in recent years. However, the underlying mechanism by which MPs have any impact on brown and beige adipocytes in the context of obesity is yet to be investigated. METHODS: The C57BL/6 J mice were randomly assigned to the HFD and HFD+MPs group for 12 weeks of exposure to explore the differences in brown and beige adipocyte function. The gut microbiota analysis, fecal microbiota transplantation and metabolomic profiling were carried out to further determine its potential mechanism. RESULTS: The present work demonstrated that high-fat diet mice accumulate lipids and have reduced energy expenditure after three months of oral administration of MPs. In addition to escalating intestinal dysbiosis, exposing HFD mice to MPs induces thermogenic dysfunction in inguinal white adipose tissue and brown adipose tissue. Following the fecal microbiota transplantation, the accumulation of lipids and dysfunction in energy expenditure within the microbiota of recipient mice further elucidated the inhibitory effect of MPs. CONCLUSIONS: Our results suggest that MPs induced the thermogenic dysfunction of BAT and iWAT by affecting gut microbiota composition. The present study highlights the mechanisms by which MPs produce thermogenic dysfunction in BAT and iWAT and disruption in the gastrointestinal microbiota.