The adverse effects of perinatal exposure to nonylphenol on carbohydrate metabolism in male offspring rats.

BACKGROUND

We sought to investigate the adverse effects of perinatal exposure to nonylphenol (NP) on carbohydrate metabolism of male offspring rats.

METHODS

Thirty-two healthy pregnant Sprague Dawley rats were randomly divided into four groups, control normal diet group (C), NP normal diet group (NPN), control high-energy diet group (CH), and NP high-energy diet group (NPH). Both of the control groups were received a gavage of corn oil and the NP-groups were received NP (200 mg/kg/day) from gestational days 6 to post-natal day (PND) 21. The concentrations of NP in pancreatic tissues were measured by high-performance liquid chromatography (HPLC). The key genes of glucose metabolism expression were detected by reverse transcription-polymerase chain reaction (RT-PCR). The pancreatic tissues were stained with hematoxylin/eosin (HE).

RESULTS

On PND 1, the body weights of male pups in the NPN and NPH groups were lower than those of the CH group (p = 0.012 and 0.001, respectively). On PND 30, the body weight of male pups from the NPH group was elevated compared with the C group (p = 0.019), while the body weights of male pups in the NPN and NPH groups were elevated compared to the CH group (p = 0.034 and 0.004, respectively). On PND 60, the body weights of NPN and NPH pups were higher than those in the C (p < 0.001) and CH groups (p < 0.001). The levels of fasting blood glucose (FBG) were increased significantly in the animals treated with NP compared to control animals (F = 29.14, p < 0.001). The FBG levels in the treatment groups are ranked as follows: NPH > NPN > CH > C (p < 0.05). The concentrations of NP in pancreas tissues in both the NPN (2045.0 ± 130.1 μg/L) and NPH groups (2038.0 ± 104.2 μg/L) were higher than those in the C (499.5 ± 27.4 μg/L) and CH groups (494.2 ± 22.4 μg/L; p < 0.05). Morphological examination of tissues from rats exposed to NP shown that the NP-treated groups appeared to have a higher degree of inflammatory injury, edema, and focal necrotic cells in the pancreatic tissues. Compared with C group, expression of glucokinase (GCK) was down-regulated, while Uncoupling protein-2 (UCP-2) was up-regulated in the NP-treated groups (FGCK = 218.89, p < 0.001; FUCP-2 = 18.82, p < 0.001).

CONCLUSIONS

Prenatal exposure to NP could induce glucose metabolism disorder in male F1 rats, which may be due to the fact that NP induces abnormal expression patterns of GCK and UCP-2.