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Oral exposure to PET microplastics alters the pancreatic transcriptome – implications for the pathogenesis of type 1 diabetes
Summary
Researchers exposed immature pigs to PET microplastics for four weeks and analyzed the resulting changes in pancreatic gene expression using RNA sequencing. They found a dose-dependent effect, with the higher dose altering expression of 86 genes including immune cell markers, cytokines, and chemokines that may activate immune responses characteristic of type 1 diabetes development. The study suggests that oral exposure to PET microplastics could be an environmental risk factor worth investigating in the context of rising type 1 diabetes incidence.
Abstract Type 1 diabetes is a chronic autoimmune disease, the incidence of which has been steadily increasing in recent years, particularly among adolescents. The disease results from a combination of genetic and environmental factors that lead to the destruction of insulin-producing beta cells in the pancreas. Recently, the potential role of microplastics in the pathogenesis of various diseases has gained attention. Therefore, the aim of this study was to investigate the impact of PET microplastics on the pancreas using immature pigs as a model organism. The global transcriptomic profile of the pancreas was analyzed in piglets treated with either a low (0.1 g/day) or high dose (1 g/day) of PET microplastics for 4 weeks using RNA-Seq. The analysis revealed a dose-dependent effect of PET microplastics on gene expression. A low dose affected the expression of one gene, while a high dose impacted the expression of 86 genes. The differentially expressed genes, including immune cell markers, cytokines and chemokines, may activate the immune system in the pancreas in a way that is characteristic of the pathogenesis of type 1 diabetes. It suggests that oral exposure to PET microplastics may be a new risk factor for the development of this disease.
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