Abstract
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.