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

• Published in: Molecular and cellular endocrinology Vol. 354; no. 1-2; pp. 74 - 84
• Main Authors: vom Saal, Frederick S., Nagel, Susan C., Coe, Benjamin L., Angle, Brittany M., Taylor, Julia A.
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 06.05.2012
• Subjects: adipocytes; Adipocytes - drug effects; Adipocytes - metabolism; Adipocytes - physiology; adults; Animals; Benzhydryl Compounds; Bisphenol A; blood flow; Endocrine disrupting chemicals; Endocrine Disruptors - toxicity; Environmental Exposure; Environmental Pollutants - toxicity; epigenetics; Estrogens - toxicity; fetal development; Fetal Development - drug effects; fetus; Gene Expression Regulation - drug effects; Humans; Metabolic syndrome; nutrient transport; Obesity; Obesity - chemically induced; Obesity - genetics; Obesity - pathology; Phenols - toxicity; Phenotype; reproductive performance; C/EBPβ; C/EBPα; Obesity; DOHaD; DGAT1; ERβ; ERα; LPL; Cyp19; GLP; Metabolic syndrome; PPARγ; Endocrine disrupting chemicals; Bisphenol A; BPA; SERMs; IUGR; GLUT4; GnRH; GPAT; HPLC
• ISSN: 0303-7207; 1872-8057; 1872-8057
• DOI: 10.1016/j.mce.2012.01.001

► Estrogenic EDC exposure may lead to obesity via genetic programming. ► Estrogens and EDCs directly regulate adipocyte function. ► Developmental EDC exposure influences adult body weight and metabolism. ► Effects of EDCs on body weight and on glucose homeostasis are seen at low doses. 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.