The estrogenic endocrine disrupting chemical bisphenol A (BPA) and obesity

Mol Cell Endocrinol. 2012 May 6;354(1-2):74-84. doi: 10.1016/j.mce.2012.01.001. Epub 2012 Jan 10.

Abstract

There is increasing experimental and epidemiological evidence that fetal programming of genetic systems is a contributing factor in the recent increase in adult obesity and other components of metabolic syndrome. In particular, there is evidence that epigenetic changes associated with the use of manmade chemicals may interact with other factors that influence fetal and postnatal growth in contributing to the current obesity epidemic. The focus of this review is on the developmental effects of estrogenic endocrine disrupting chemicals (EDCs), and more specifically on effects of exposure to the estrogenic EDC bisphenol A (BPA), on adipocytes and their function, and the ultimate impact on adult obesity; BPA exposure also results in impaired reproductive capacity. We discuss the interaction of EDCs with other factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, and how these influence fetal growth and abnormalities in homeostatic control systems required to maintain normal body weight throughout life.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adipocytes / drug effects
  • Adipocytes / metabolism
  • Adipocytes / physiology
  • Animals
  • Benzhydryl Compounds
  • Endocrine Disruptors / toxicity*
  • Environmental Exposure
  • Environmental Pollutants / toxicity*
  • Estrogens / toxicity*
  • Fetal Development / drug effects
  • Gene Expression Regulation / drug effects
  • Humans
  • Obesity / chemically induced*
  • Obesity / genetics
  • Obesity / pathology
  • Phenols / toxicity*
  • Phenotype

Substances

  • Benzhydryl Compounds
  • Endocrine Disruptors
  • Environmental Pollutants
  • Estrogens
  • Phenols
  • bisphenol A