Perfluorooctanoic acid impaired glucose homeostasis through affecting adipose AKT pathway.

Perfluorooctanoic acid (PFOA) is commonly applied in manufactured products, and its potential health risk is concerned greatly. Increasing evidences have indicated PFOA-induced liver dysfunction. However, detailed molecular mechanism has not been completely identified. In this study, we aimed to investigate the mechanical association between PFOA exposure and AKT pathway in white adipose tissue. As results, PFOA-treated mice showed increased blood glucose and insulin levels, and induced insulin resistance. In addition, serum levels of leptin and adiponectin in PFOA-treated mice were elevated. As shown in histological examination, increased cell death counts in PFOA-treated adipose were observed, as well as ultrastructural impairment in adipose cells was found. Further, immunohistochemical stains exhibited GLUT4, p-AKT positive cells were down-regulated in PFOA-treated adipose, while PTEN immune-labeled cells were reduced. In validated data, RT-PCR assay suggested adipose AKT mRNA was down-regulated in PFOA-treated mice, and PTEN mRNA was increased. Western blot data showed that intracellular PTEN protein level in PFOA-treated adipose was up-regulated, while phosphorylation of AKT, GSK3β levels were lowered dose-dependently. Taken together, the present findings indicate that PFOA impaired glucose homeostasis via negatively regulating AKT pathway in white adipose tissue.