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Adipocyte and Cell Biology

The environmental obesogen bisphenol A promotes adipogenesis by increasing the amount of 11β-hydroxysteroid dehydrogenase type 1 in the adipose tissue of children

International Journal of Obesity volume 37, pages 999–1005 (2013)Cite this article

Subjects

Abstract

Background:

Bisphenol A (BPA) is considered as an environmental obesogen. The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts the inactive hormone cortisone to the active hormone cortisol in adipose tissues and promotes adipogenesis.

Objective:

To examine whether environmentally relevant concentrations of BPA could increase the expression of 11β-HSD1, as well as that of the adipogenesis-related genes peroxisome proliferator-activated receptor-γ (PPAR-γ) and lipoprotein lipase (LPL), in the adipose tissue of children.

Methods:

Omental fat biopsies were obtained from 17 children (7 boys and 10 girls between 3 and 13 years of age) undergoing abdominal surgery. The effects of BPA (10 nM, 1 μM, and 80 μM) on 11β-HSD1, PPAR-γ and LPL mRNA expression, and 11β-HSD1 enzymatic activity in adipose tissue and adipocytes were assessed in vitro. Moreover, the effects of carbenoxolone (CBX), an 11β-HSD1 inhibitor, or RU486, a glucocorticoid (GC) receptor antagonist, on 11β-HSD1, PPAR-γ and LPL mRNA expression were assessed in human visceral preadipocytes and adipocytes.

Results:

BPA, even at the lowest concentration tested (10 nM), increased the mRNA expression and enzymatic activity of 11β-HSD1 in the omental adipose tissue samples and the visceral adipocytes. Similar effects on PPAR-γ and LPL mRNA expression and lipid accumulation were observed in the adipocytes. CBX treatment inhibited the stimulatory effects of BPA (at 10 nM) on PPAR-γ and LPL mRNA expression, whereas RU486 inhibited 11β-HSD1 mRNA expression in the adipocytes.

Conclusion:

BPA, at environmentally relevant levels, increased the mRNA expression and enzymatic activity of 11β-HSD1 by acting upon a GC receptor, which may lead to the acceleration of adipogenesis.

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Acknowledgements

This work was supported through funding from 973 Program of China (2013CB530604), the National Natural Science Foundation of China (81273064), the Blue Project of the Jiangsu Education Department of China (JX10410533), the Scientific Research Foundation for Returned Overseas Scholars of the Ministry of Education of China (DG216G15013), and the Project Funder by the Priority Academic Program Development of Jiangsu Higher Education Institutions. We thank the doctors in the Department of Surgery at Nanjing Children’s Hospital for collecting samples, Associate Professor Baoqing Mo (Department of Public Health, Nanjing Medical University) for help with statistical analysis, and Professor Duan Chen (Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology) for valuable discussions.

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Authors and Affiliations

  1. Department of Children’s Health Care, Nanjing Children’s Hospital Nanjing Medical University, Nanjing,, China

    J Wang, M Hou & X Li

  2. Department of General Surgery, Nanjing Children’s Hospital Nanjing Medical University, Nanjing,, China

    B Sun

  3. Institute of Pediatric Research, Nanjing Children’s Hospital, Nanjing Medical University, Nanjing,, China

    X Pan & X Li

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Correspondence to X Li.

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Wang, J., Sun, B., Hou, M. et al. The environmental obesogen bisphenol A promotes adipogenesis by increasing the amount of 11β-hydroxysteroid dehydrogenase type 1 in the adipose tissue of children. Int J Obes 37, 999–1005 (2013). https://doi.org/10.1038/ijo.2012.173

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