Developmental exposure to endocrine disruptors and the obesity epidemic

Newbold, Retha R.; Padilla-Banks, Elizabeth; Snyder, Ryan J.; Phillips, Terry M.; Jefferson, Wendy N.

doi:10.1016/j.reprotox.2006.12.010

Cited by 226 publications

(191 citation statements)

References 22 publications

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“…These results suggest that attention should also be paid to T-cell differentiation in the female thymus in research on EDCs. Early onset of sexual maturation was reported in female mice delivered from dams treated with low doses of BPA (20 μg/kg/day) during gestation (Newbold et al, 2007;Honma et al, 2002). However, early onset of sexual maturation was not observed in mice neonatally treated with BPA (5 and 50 μg/kg) in the present study.…”

Section: Discussioncontrasting

confidence: 79%

“…Although increased body weight in mice after exposure to low doses of BPA (Rubin et al, 2001) or DES (Newbold et al, 2007) has been reported, decreased body weight was observed in male mice after neonatal exposure to low doses of BPA in this study. When the body weights of the male mice were compared to the background data we have on the same strain, the data of the control group in the present study were relatively high and those of the BPA groups were similar to the background data.…”

Section: Discussioncontrasting

confidence: 77%

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Normal ovarian aging, but modified T-cell differentiation, in female mice following neonatal exposure to bisphenol A

Ohta

Ohmukai

Negura

et al. 2017

Fundam. Toxicol. Sci.

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-In a previous study, we found that early life exposure to low-dose diethylstilbestrol accelerated onset of abnormal estrous cycles in female C57BL/6J mice. In order to observe the ovarian aging of mice exposed to substances on the candidate list for endocrine-disrupting properties, neonates of C57BL/6J mice were orally administered bisphenol A (BPA) at doses of 5 and 50 μg/kg/day. As a result, normal ovarian aging was observed in females treated with BPA. However, females treated with 5 and 50 μg/kg/day of BPA showed modified T-cell differentiation in the thymus. These results suggested that early life exposure to low-dose BPA did not induce premature ovarian failure but modified T-cell differentiation in female mice.

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Section: Discussioncontrasting

confidence: 79%

Section: Discussioncontrasting

confidence: 77%

Normal ovarian aging, but modified T-cell differentiation, in female mice following neonatal exposure to bisphenol A

Ohta

Ohmukai

Negura

et al. 2017

Fundam. Toxicol. Sci.

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“…Neonatal exposure to DES is reported to cause increase of uterine weight [30], decrease of body weight [31], and later in life, obesity [31] and uterine cancer [32]. One of the objectives of our work was to detect epigenetic changes in young mice to predict a future disease.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Exposure to Diethylstilbestrol Alters Expression of DNA Methyltransferases and Methylation of Genomic DNA in the Mouse Uterus

et al. 2009

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Abstract. Perinatal exposure to diethylstilbestrol (DES) can have numerous adverse effects on the reproductive organs later in life, such as vaginal clear-cell adenocarcinoma. Epigenetic processes including DNA methylation may be involved in the mechanisms. We subcutaneously injected DES to neonatal C57BL/6 mice. At days 5, 14, and 30, expressions of DNA methyltransferases (Dnmts) Dnmt1, Dnmt3a, and Dnmt3b, and transcription factors Sp1 and Sp3 were examined. We also performed restriction landmark genomic scanning (RLGS) to detect aberrant DNA methylation. Real-time RT-PCR revealed that expressions of Dnmt1, Dnmt3b, and Sp3 were decreased at day 5 in DES-treated mice, and that those of Dnmt1, Dnmt3a, and Sp1 were also decreased at day 14. RLGS analysis revealed that 5 genomic loci were demethylated, and 5 other loci were methylated by DES treatment. Two loci were cloned, and differential DNA methylation was quantified. Our results indicated that DES altered the expression levels of Dnmts and DNA methylation. [3][4][5], and DES is now widely known as an estrogenic endocrine disruptor. In our previous studies, we showed that mice treated neonatally with DES or the phytoestrogen, genistein, developed altered expression levels of various genes in male reproductive organs, even during adulthood [6][7][8][9][10]. Since the expression changes lasted for long periods of time, and DES was reported to be non-genotoxic [11], epigenetic mechanisms might be involved in the gene expression changes. DNA methylation has an important role in epigenetics, and the DNA methy-

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“…Additionally, there are genetic components for developing obesity. Lately, it has been hypothesized that exposure to endocrine disruptors, in utero and onwards, may play a role in the development of obesity and related diseases (Baillie-Hamilton 2002, Newbold et al 2007bNewbold et al , 2008. The molecular mechanisms behind a possible involvement of EDCs, so called obesogens, in obesity are poorly understood.…”

Section: Is Exposure To Edcs Involved In Development Of Metabolic Dismentioning

confidence: 99%

Endocrine disruptive chemicals: mechanisms of action and involvement in metabolic disorders

Swedenborg¹,

Rüegg²,

Mäkelä³

et al. 2009

Journal of Molecular Endocrinology

254

160

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Endocrine disruption refers to the ability of chemicals to interfere with hormonal systems, and has raised considerable concern in recent years. Endocrine disruptive chemicals (EDCs) pose a documented risk to wildlife and have the potential to negatively influence human health. This review focuses on the molecular mechanisms of endocrine disruption and the possible involvement of EDCs in metabolic disorders. The first part describes the role of aryl hydrocarbon receptor (AhR) and nuclear receptors (NRs) in mediating effects of EDCs, in particular, how cross-talk between AhR and NR pathways can lead to endocrine disruption. The second part deals with how these receptors are involved in metabolic functions and how their targeting by EDCs can lead to disturbances in glucose and fat metabolism. The article illustrates that, although there is accumulating data on molecular mechanisms of EDC action as well as on EDC involvement in metabolic disorders, there is still a great demand for data that can unite the mechanistic and the toxicological /epidemiological observations.

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Developmental exposure to endocrine disruptors and the obesity epidemic

Cited by 226 publications

References 22 publications

Normal ovarian aging, but modified T-cell differentiation, in female mice following neonatal exposure to bisphenol A

Normal ovarian aging, but modified T-cell differentiation, in female mice following neonatal exposure to bisphenol A

Neonatal Exposure to Diethylstilbestrol Alters Expression of DNA Methyltransferases and Methylation of Genomic DNA in the Mouse Uterus

Endocrine disruptive chemicals: mechanisms of action and involvement in metabolic disorders

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