Keywords: 
• PFOS /
• glucose metabolism /
• developmental toxicity

Abstract: Effect of perinatal exposure to PFOS on glucose metabolism of adult rat offsprings was investigated. The pregnant rats were exposed to PFOS with doses of 0 mg·kg^-1 PFOS (control), 4 mg·kg^-1 PFOS (low) or 8 mg·kg^-1 PFOS (high) through diet from gestation day 0 (GD 0) to postnatal day 21 (PND21). Serum PFOS concentrations were determined on PND1, PND21 and PND42 by HPLC-LC/MS. The rats' body weight was monitored during the experiments. Fasting blood glucose and fasting serum insulin level were measured at 8 and 18 weeks after weaning. Homeostasis model assessment insulin resistance index (HOMA-IR) was also calculated. Moreover, oral glucose tolerance test (OGTT) was performed on 18 weeks in male offspring after weaning and the area under curve was calculated. Besides, expression of glucose metabolism-related genes was measured using real-time PCR. The present study showed that serum PFOS concentration increased after exposure and the concentration was highest on PND 21, with (7.77 ±1.45) μg·mL^-1 at 4 mg·kg^-1 dose and (5.09 ±0.57) μg·mL^-1 at 8 mg·kg^-1 dose. Additionally, body weights of rat pups from PFOS exposure groups were significantly lower than control group. Though the fasting blood glucose levels were affected by PFOS only in male offspring, serum insulin levels were significantly elevated in all exposure groups. The degree of insulin resistance was also elevated and PFOS exposure could impair the glucose tolerance of male rat pups at 18 week. Furthermore, results from RT-PCR revealed that PFOS up-regulated the expression level of PGC-1 and PEPCK, while down-regulated the expression level of hypoglycemic gene G6P. In conclusion, developmental exposure to PFOS disturbed the glucose homeostasis of rat pups in the adulthood, led to insulin resistance and increased the risk of diabetes and metabolic disorder.