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The effect and a mechanistic evaluation of polystyrene nanoplastics on a mouse model of type 2 diabetes
Summary
Researchers found that polystyrene nanoplastics worsened type 2 diabetes symptoms in mice, including blood sugar control, insulin resistance, and organ damage in the liver and pancreas. Even nanoplastics alone, without a high-fat diet, caused significant increases in blood glucose and insulin resistance at higher doses. The study reveals a specific molecular pathway through which nanoplastics disrupt blood sugar regulation, raising concerns that chronic human exposure to nanoplastics could contribute to metabolic diseases like diabetes.
Nanoplastics have become ubiquitous in the global environment and have attracted increasing attention. However, whether there is an influence between exposure to nanoplastics and diabetes is unclear. To determine the effects of exposure to Polystyrene nanoplastics (PS-NPs) and evaluate the underlying mechanisms, mice were orally exposed to PS-NPs at dosages of 1, 10, 30 mg/kg/day for 8 weeks, alone or combined with a high fat diet and streptozocin (STZ) injection. Our data showed that exposure to 30 mg/kg/day PS-NPs alone induced a significant increase in blood glucose, glucose intolerance and insulin resistance. Combined with a high fat diet and STZ injection, PS-NPs exposure markedly aggravated oxidative stress, glucose intolerance, insulin tolerance and insulin resistance, and induced lesions in the liver and pancreas. PS-NPs exposure could decrease the phosphorylation of AKT and GSK3β, and treatment with SC79, a selective AKT activator, could increase the level of AKT and GSK3β phosphorylation, effectively alleviating the increase in ROS levels in the liver or pancreas, and slightly attenuating the increase in fasting blood glucose levels and insulin resistance induced by PS-NPs exposure. This showed that exposure to PS-NPs aggravated type 2 diabetes and the underlying mechanism partly involved in the inhibition of AKT/GSK3β phosphorylation.