Long-term oral exposure to bisphenol A induces glucose intolerance and insulin resistance

  1. Kyong Soo Park1
  1. 1Department of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Republic of Korea
    2Department of Internal Medicine, Boramae Medical Center, Seoul 156-707, Republic of Korea
    3Department of Internal Medicine, Chung-Ang University Hospital, College of Medicine, Chung-Ang University, Seoul 156-755, Republic of Korea
    4Clinical Research Institute, Seoul National University Hospital, Seoul 110-74, Republic of Korea
    5Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam 463-707, Republic of Korea
  1. Correspondence should be addressed to Y J Park; Email: yjparkmd{at}snu.ac.kr
  1. Figure 1

    Long-term exposure to bisphenol A in growing mice had no effect on body weight or fat mass. (A) Growth curves in mice that received standard chow diet (CD) (open circle), CD+bisphenol A (BPA) (open square), high-fat diet (HFD) (filled circle), or HFD+BPA (filled square). (B) Body weight. (C) Percentage of white adipose tissue (WAT). (D) Percentage of body fat. Data are presented as means±s.e.m. Bwt, body weight; CON, control; BPA, bisphenol A; DXA, dual-energy X-ray absorptiometry.

  2. Figure 2

    Long-term exposure to bisphenol A induced glucose intolerance in mice that received a high-fat diet (HFD). (A) Intraperitoneal glucose tolerance tests (IPGTTs) (d-glucose: 2 g/kg body weight) were performed in 16- to 18-week-old male mice that received standard chow diet (CD) (open circle), CD+bisphenol A (BPA) (open square), HFD (filled circle), or HFD+BPA (filled square). (B) Fasting insulin levels. Data are presented as means±s.e.m. *P<0.05. CON, control; BPA, bisphenol A.

  3. Figure 3

    Long-term exposure to bisphenol A impaired insulin signaling in skeletal muscle. (A) Protein analysis of Akt phosphorylation at positions Thr308 and Ser473 in skeletal muscle. (B) Densitometry of Akt phosphorylation at position Thr308. *P<0.05. (C) Protein analysis of GSK3β protein levels and its phosphorylation at position Ser9 in skeletal muscle. (D) Densitometry of GSK3β phosphorylation at position Ser9. *P<0.05. HFD, high-fat diet; BPA, bisphenol A.

  4. Figure 4

    Bisphenol A tended to decrease serum adiponectin levels and increase serum interleukin 6 (IL6) and tumor necrosis factor α (TNFα) levels. (A) Serum adiponectin levels. (B) Serum IL6 levels. (C) Serum TNFα levels. Data are presented as means±s.e.m. HFD, high-fat diet; BPA, bisphenol A.

  5. Figure 5

    Long-term exposure to bisphenol A did not induce any detrimental changes in the islet cell area or morphology or the insulin content of β cells. (A) Percentage of islet cell area. (B) Percentage of insulin content in pancreatic tissue. Data are presented as means±s.e.m. (C) Pancreatic islet cell morphology by electron microscopy in mice fed a high-fat diet (HFD) only (50 000× magnification). (D) Pancreatic islet cell morphology in mice fed an HFD and bisphenol A (BPA) (50 000× magnification).

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