The prevalence of obesity and its related disorders is currently attaining pandemic proportions, both in the Western and the developing world. Although life choices are commonly accepted as the main reasons, it has recently been suggested that environmental pollutants may provide an alternative cause. Several man-made chemicals have been shown to facilitate the differentiation into adipocyte at environmentally relevant levels. This process is mediated through different nuclear receptors. The endocrine function of the adipocyte itself is also affected by chemicals. This article provides a compact overview of the implicated chemicals and their modes of action. We also present the current level of evidence, linking exposure to these endocrine disrupting chemicals and obesity and its related diseases.
 Cameron, A.J. et al. (2012) A systematic review of the impact of including both waist and hip circumference in risk models for cardiovascular diseases, diabetes and mortality. Obesity Reviews, 41, 484-494.
 Matthiessen, P., et al. (1995) Changes in periwinkle (Littorina littorea) populations following the ban on TBT-ba- sed antifoulings on small boats in the United Kingdom. Ecotoxicology and Environmental Safety, 30, 180-194.
 Vos, J.G., et al. (2000) Health effects of endocrine-disru- pting chemicals on wildlife, with special reference to the European situation. Critical Reviews in Toxicology, 30, 71-133. doi:10.1080/10408440091159176
 Ballschmite, K., et al. (2002) Man-made chemicals found in remote areas of the world: the experimental definition for POPs. Environmental Science and Pollution Research, 9, 274-88. doi:10.1007/BF02987503
 Pedersen, S.B., et al. (2004) Estrogen controls lipolysis by up-regulating alpha2A-adrenergic receptors directly in human adipose tissue through the estrogen receptor alpha. Implications for the female fat distribution. The Journal of Clinical Endocrinology & Metabolism, 89, 1869-1878.
 Rubin, B.S., et al. (2001) Perinatal exposure to low doses of bisphenol A affects body weight, pat-terns of estrous cyclicity, and plasma LH levels. Environmental Health Perspectives, 109, 675-680.
 Penza, M., et al. (2011) The environmental chemical tri- butyltin chloride (TBT) shows both estrogenic and adi- pogenic activities in mice which might depend on the ex-posure dose. Toxicology and Applied Pharmacology, 255, 65-75.
 Lehmann, J.M. (1995) An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-acti- vated receptor gamma (PPAR gamma). The Journal of Biological Chemistry, 270, 12953-12956.
 Liu, S.C. (2012) Effect of antidiabetic agents added to metformin on glycaemic control, hypoglycaemia and weight change in patients with type 2 diabetes: A network meta-analysis. Diabetes, Obesity and Metabolism, 14, 810- 820.
 Tchoukalova, Y.D., et al. (2012) In vivo adipogenesis in rats measured by cell kinetics in adipocytes and plastic-adherent stroma-vascular cells in response to high-fat diet and thiazolidinedione. Diabetes, 61, 137-144.
 Kanayama, T., et al. (2005) Organotin compounds pro- mote adipocyte differentiation as agonists of the perox- isome prolifera-tor-activated receptor gamma/retinoid X receptor pathway. Molecular Pharmacology, 67, 766-774.
 Bility, M.T., et al. (2004) Activation of mouse and human peroxisome proliferator-activated receptors (PPARs) by phthalate monoesters. Society of Toxicology, 82, 170-182. doi:10.1093/toxsci/kfh253
 Feige, J.N., et al. (2007) The endocrine disruptor mono- ethyl-hexyl-phthalate is a selective peroxisome prolifera- tor-activated receptor gamma modulator that promotes adipogenesis. The Journal of Biological Chemistry, 282, 19152-19166. doi:10.1074/jbc.M702724200
 Stahlhut, R.W., et al. (2007) Concentrations of urinary phthalate metabolites are associated with increased waist circumference and insulin resistance in adult US males. Environmental Health Perspectives, 115, 876-882.
 Hatch, E.E., et al. (2008) Association of urinary phthalate metabolite concentrations with body mass index and waist circumference: A cross-sectional study of NHANES data, 1999-2002. Environmental Health, 3, 27.
 Wauters, M., et al. (2001) Polymorphisms in the leptin receptor gene, body composition and fat distribution in overweight and obese women. International Journal of Obesity and Related Metabolic Disorders, 25, 714-720.
 Hugo, E.R., et al. (2008) Bisphenol A at environmentally relevant doses inhibits adiponectin release from human adipose tissue explants and adipocytes. Environmental Health Perspectives, 116, 1642-1647.
 Heindel, J.J. and vom Saal, F.S. (2009) Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity. Molecular and Cellular Endocrinology, 304, 90-96.
 Beyerlein, A., et al (2011) Is low birth weight in the causal pathway of the associa-tion between maternal smo- king in pregnancy and higher BMI in the offspring? European Journal of Epidemiology, 26, 413-420.
 Karmaus, W., et al. (2009) Maternal levels of dichlorodiphenyl-dichloroethylene (DDE) may increase weight and body mass index in adult female offspring. Occupational and Environmental Medicine, 66, 143-149.
 Elobeid, M.A., et al. (2010) Endocrine disruptors and obesity: An examination of selected persistent organic pol- lutants in the NHANES 1999-2002 data. International Journal of Environmental Research and Public Health, 7, 2988-3005.
 Everett, C.J., et al. (2007) Association of a polychlori- nated dibenzo-p-dioxin, a polychlorinated biphenyl, and DDT with diabetes in the 1999-2002 National Health and Nutrition Examination Survey. Environmental Research, 103, 413-418.
 Lee, D.-H., et al. (2006) A strong dose-response relation between serum concentrations of persistent organic pollu- tants and diabetes: Results from the National Health and Examination Survey 1999-2002. Diabetes Care, 29, 1638- 1644. doi:10.2337/dc06-0543
 Lee, D.-H., et al. (2010) Low dose of some persistent organic pollutants predicts type 2 diabetes: A nested case- control study. Environmental Health Perspectives, 118, 1235-1242. doi:10.1289/ehp.0901480
 Lee, D.H., et al. (2007) Relationship between serum con- centrations of persistent organic pollutants and the prevalence of metabolic syndrome among non-diabetic adults: results from the National Health and Nutri-tion Examina- tion Survey 1999-2002. Diabetologia, 50, 1841-1851.
 Gladen, B.C., et al. (2000) Pubertal growth and development and prenatal and lactational exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene. Journal of Pediatrics, 136, 490-496. doi:10.1016/S0022-3476(00)90012-X
 Welshons, W.V., et al. (2006) Large effects from small exposures. III. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Endocrinol- ogy, 147, S56-S69. doi:10.1210/en.2005-1159