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Effect of Nonylphenol on Adiposity and Glucose Homeostasis in Mice with Diet Induced Obesity
Author(s) -
Ribeiro Carolina Martins,
Oliveira Fernanda Cerqueira Barroso,
Pereira Sidney Alcântara,
Assis Rocha Neves Francisco,
Coelho Michella Soares,
Amato Angélica Amorim
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.886.2
Subject(s) - medicine , endocrinology , glucose homeostasis , adipose tissue , white adipose tissue , lipogenesis , homeostasis , energy homeostasis , nonylphenol , brown adipose tissue , obesity , chemistry , biology , insulin resistance , environmental chemistry
Nonylphenol (NP) is the predominant environmental biodegradation product of NP ethoxylates and is widely use in detergents, plastic products and paints. It is an endocrine disrupter found to compete with 17β‐estradiol for the binding site of estrogen receptor, due to their structural similarity. More recently, it was also identified as an environmental obesogenic, both in cell culture and in vivo. Acute exposure to NP has been found to induce the expression of adipogenesis and lipogenesis‐related genes in adipose tissue. Additionally, perinatal exposure to different concentrations of NP has resulted in increased body mass and adiposity in male and female offspring. However, the obesogenic potential of long‐term exposure to NP outside the perinatal period has not been investigated. Objective To investigate the effects of chronic exposure to NP on body weight, adiposity and glucose homeostasis in female C57BL/6 mice. Methods Female C57BL/6 mice were fed a high‐fat diet (HFD, 60% kcal as fat) from the 5 th to 20 th week of age. The animals were randomly divided into five groups (n=6) and treated with vehicle (drinking water) or NP 0.5 mg/kg/d or 2.5 mg/kg/d for 16 weeks (5 th to 20 th wk) or for 6 weeks (14 th to 20 th wk) in drinking water. Weight, weight gain, food and water consumption were measured. Two different white adipose tissue (WAT‐retroperitoneal and perigonadal) and one interscapular brown adipose tissue (BAT) depots were weighed. Glucose homeostasis was assessed by fasting glucose levels, glucose tolerance test (GTT), and insulin tolerance test (ITT). Results There was a slight, but nonsignificant trend towards increased body weight and weight gain in response to NP treatment at doses of 0.5 mg/kg/d for 6 or 16 weeks and 2.5 mg/kg/d for 16 weeks when compared to vehicle. On the other hand, mice treated with NP 2.5 mg/kg/d for 6 weeks showed a trend towards decreased body weight. Treatment with NP did not affect energy intake, but increased water consumption when compared to vehicle. Fasting glucose levels at the 20 th week were nonsignificantly decreased by NP treatment (0.5 mg/kg/d, 6 wk). However, there were no changes in glucose tolerance or insulin sensitivity. Visceral WAT, subcutaneous WAT and BAT mass remained unchanged in response to treatment with NF. Conclusions Our findings suggest long‐term exposure of female mice to environmentally relevant NP concentrations, outside of the developmental period, does not affect glucose homeostasis or adiposity. Support or Funding Information CNPq/CAPES/FAPDF