Effects of endocrine disruptors on obesity

被引:240
作者
Newbold, Retha R. [1 ]
Padilla-Banks, Elizabeth [1 ]
Jefferson, Wendy N. [1 ]
Heindel, Jerrold J. [2 ]
机构
[1] NIEHS, Dev Endocrinol & Endocrine Disruptor Sect, Mol Toxicol Lab, Div Intramural Res, Res Triangle Pk, NC 27709 USA
[2] NIEHS, Div Extramural Res, Res Triangle Pk, NC 27709 USA
来源
INTERNATIONAL JOURNAL OF ANDROLOGY | 2008年 / 31卷 / 02期
关键词
adipocytes; environmental estrogens; leptin; metabolic disease; obesogens; xenoestrogens;
D O I
10.1111/j.1365-2605.2007.00858.x
中图分类号
R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
摘要
Environmental chemicals with hormone-like activity can disrupt the programming of endocrine signalling pathways that are established during perinatal life and result in adverse consequences that may not be apparent until much later in life. Increasing evidence implicates developmental exposure to environmental hormone mimics with a growing list of adverse health consequences in both males and females. Most recently, obesity has been proposed to be yet another adverse health effect of exposure to endocrine disrupting chemicals (EDCs) during critical stages of development. Obesity is quickly becoming a significant human health crisis because it is reaching epidemic proportions worldwide, and is associated with chronic illnesses such as diabetes and cardiovascular disease. In this review, we summarize the literature reporting an association of EDCs and the development of obesity, and further describe an animal model of exposure to diethylstilbestrol that has proven useful in studying mechanisms involved in abnormal programming of various oestrogen target tissues during differentiation. Together, these data suggest new targets (i.e. adipocyte differentiation and mechanisms involved in weight homeostasis) of abnormal programming by EDCs, and provide evidence that support the scientific term 'the developmental origins of adult disease'. The emerging idea of an association of EDCs and obesity expands the focus on obesity from intervention and treatment to include prevention and avoidance of these chemical modifiers.
引用
收藏
页码:201 / 207
页数:7
相关论文
共 41 条
[1]   Low doses of bisphenol A and diethylstilbestrol impair Ca2+ signals in pancreatic α-cells through a nonclassical membrane estrogen receptor within intact islets of Langerhans [J].
Alonso-Magdalena, P ;
Laribi, O ;
Ropero, AB ;
Fuentes, E ;
Ripoll, C ;
Soria, B ;
Nadal, A .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2005, 113 (08) :969-977
[2]   Chemical toxins: A hypothesis to explain the global obesity epidemic [J].
Baillie-Hamilton, PF .
JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE, 2002, 8 (02) :185-192
[3]   Fetal origins of adult disease:: strength of effects and biological basis [J].
Barker, DJP ;
Eriksson, JG ;
Forsén, T ;
Osmond, C .
INTERNATIONAL JOURNAL OF EPIDEMIOLOGY, 2002, 31 (06) :1235-1239
[4]  
BERN HA, 1992, CHEM INDUCED ALTERAT, P9
[5]  
CARBON T, 1992, CHEM INDUCED ALTERAT
[6]   DEVELOPMENTAL EFFECTS OF ENDOCRINE-DISRUPTING CHEMICALS IN WILDLIFE AND HUMANS [J].
COLBORN, T ;
SAAL, FSV ;
SOTO, AM .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1993, 101 (05) :378-384
[7]  
Colborn T., 1996, OUR STOLEN FUTURE
[8]   Overview of clinical perspectives and mechanisms of obesity [J].
Collins, S .
BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY, 2005, 73 (07) :470-471
[9]   Peroxisome proliferator-activated receptor γ (PPARγ) as a molecular target for the soy phytoestrogen genistein [J].
Dang, ZC ;
Audinot, V ;
Papapoulos, SE ;
Boutin, JA ;
Löwik, CWGM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (02) :962-967
[10]  
*DHHS, 2005, SURG GEN CALL ACT PR