Researchers at the Texas A&M College of Veterinary Medicine and Biomedical Sciences announced on Aug. 3 that exposure to polyethylene microplastics may contribute to the development and progression of fatty liver disease, especially when combined with an unhealthy diet.
The study found that polyethylene, one of the world's most common plastics, increased signs of fatty liver disease in laboratory models. The effect was more pronounced when exposure was paired with a diet high in fat, fructose, and cholesterol. Polyethylene is widely used in food packaging, plastic wraps, storage containers, and beverage cup linings.
Lead researcher Surya Joshi said that individuals who consume a Western-style diet—including foods like burgers and sodas—may have a greater chance of progressing to fatty liver disease if they are also exposed to polyethylene. "Those who have a more Western-style diet, including foods like burgers and sodas, may have a greater chance of progressing to fatty liver disease if they are also exposed to polyethylene," Joshi said.
The team collaborated with researchers at the University of Oklahoma using spatial transcriptomics technology to examine gene expression within intact tissue samples. This approach allowed them to identify specific areas of liver damage caused by polyethylene exposure. The research revealed that polyethylene activates PPAR-alpha—a protein known for regulating fat production in the liver—as well as ANXA2, a gene involved in tissue repair.
Joshi said identifying these pathways could help explain how polyethylene influences liver health and potentially lead scientists toward new therapeutic strategies. "This is the pioneering study showing that polyethylene can contribute to fatty liver disease, and the use of spatial transcriptomics has determined exactly where the damage has happened within the liver," Joshi said.
The research team plans further studies into whether polyethylene contributes to later stages of liver disease such as fibrosis and aims to explore additional molecular pathways involved in response to microplastic exposure.
