Perinatal exposure to low-dose 2,2′,4,4′-tetrabromodiphenyl ether affects growth in rat offspring: What is the role of IGF-1?

Suvorov, Alexander; Battista, Marie-Claude; Takser, Larissa

doi:10.1016/j.tox.2009.03.018

Cited by 85 publications

(72 citation statements)

References 48 publications

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“…Also increased levels of several adipogenic genes were found after BDE-47 exposure, including Lep, but no changes in DNA methylation of the leptin promoter were found (36). Though perinatal exposure to BDE-47 resulted in increased body weight in rodents (37), to our knowledge, epigenetic analysis linking developmental exposure to the obesogenic effects of BDE-47 in vivo has not been performed.…”

Section: Obesogenic Edc Exposure and Epigenetic Effectsmentioning

confidence: 91%

The Role of Epigenetics in the Latent Effects of Early Life Exposure to Obesogenic Endocrine Disrupting Chemicals

Stel

Legler

2015

Endocrinology

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Recent research supports a role for exposure to endocrine-disrupting chemicals (EDCs) in the global obesity epidemic. Obesogenic EDCs have the potential to inappropriately stimulate adipogenesis and fat storage, influence metabolism and energy balance and increase susceptibility to obesity. Developmental exposure to obesogenic EDCs is proposed to interfere with epigenetic programming of gene regulation, partly by activation of nuclear receptors, thereby influencing the risk of obesity later in life. The goal of this minireview is to briefly describe the epigenetic mechanisms underlying developmental plasticity and to evaluate the evidence of a mechanistic link between altered epigenetic gene regulation by early life EDC exposure and latent onset of obesity. We summarize the results of recent in vitro, in vivo, and transgenerational studies, which clearly show that the obesogenic effects of EDCs such as tributyltin, brominated diphenyl ether 47, and polycyclic aromatic hydrocarbons are mediated by the activation and associated altered methylation of peroxisome proliferator-activated receptor-γ, the master regulator of adipogenesis, or its target genes. Importantly, studies are emerging that assess the effects of EDCs on the interplay between DNA methylation and histone modifications in altered chromatin structure. These types of studies coupled with genome-wide rather than gene-specific analyses are needed to improve mechanistic understanding of epigenetic changes by EDC exposure. Current advances in the field of epigenomics have led to the first potential epigenetic markers for obesity that can be detected at birth, providing an important basis to determine the effects of developmental exposure to obesogenic EDCs in humans.

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Section: Obesogenic Edc Exposure and Epigenetic Effectsmentioning

confidence: 91%

The Role of Epigenetics in the Latent Effects of Early Life Exposure to Obesogenic Endocrine Disrupting Chemicals

Stel

Legler

2015

Endocrinology

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“…Prenatal exposure to low doses of BDE-99 (2,2´,4,4´,5-penta-BDE) increased mouse birth weight (60), while perinatal exposure to BDE-47 (2,2´,4,4´-tetra-BDE) increased rat body weights from birth to puberty (61).…”

Section: Obesogen E Ectmentioning

confidence: 99%

Adipose tissue accumulation of endocrine disrupting compounds: Variant of a common theme in exposome research

et al. 2014

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Today, a wide variety of exogenous agents (xenobiotics) collectively termed endocrine disrupting compounds (EDC) includes almost 1000 synthetic chemicals. The group of EDC is highly heterogeneous and embodies chemicals used as industrial solvents and their by-products (persistent organic pollutants and dioxins), plastics (bisphenol A) and various pesticides, herbicides and industrial pollutions. The concept of endocrine disruption refers to exogenous chemicals present in the environment, including the food and drugs, that a ect human's hormonal systems. Both epidemiological and experimental evidence suggest an association between exposure to EDC and diabetes and related cardiometabolic disorders. These compounds are not just accumulate in the white adipose tissue, but also release into the blood circulation and exhibit their pathogenic e ects on various organs. The present review is focused on the factors in uencing the accumulation, metabolism and release of EDC in the white adipose tissue. 2014; 6: 15-22 Adipobiology

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“…Their ability to persist, bioaccumulate, and biomagnify has resulted in chronic and prolonged exposure despite the voluntary cessation of penta- and octaBDE manufacturing in the United States in 2004. PBDEs have been associated with weight gain in animal studies (Bondy et al 2013; Dufault et al 2005; Fernie et al 2006; Gee and Moser 2008; Suvorov et al 2009). PBDEs have been reported to increase adipocyte differentiation, decrease glucose oxidation, disturb glucose homeostasis, and alter gene expression in the metabolic pathways by directly interacting with retinoic X receptor (RXR), a key regulatory transcription factor in the adipogenic pathway in vertebrates (Bastos Sales et al 2013; Hoppe and Carey 2007; Kamstra et al 2014; Suvorov and Takser 2010; Tung et al 2014).…”

Section: Introductionmentioning

confidence: 99%

“…Insults to the developing fetus by endocrine disruptors may influence offspring growth. Plasma insulin-like growth factor 1 (IGF-1) was elevated in male rats perinatally exposed to low doses of BDE-47 (Suvorov et al 2009). IGF-1 gene expression alteration has been shown to play a role in glucose metabolism and gestational programming of obesity (Ross et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Prenatal Polybrominated Diphenyl Ether Exposure and Body Mass Index in Children Up To 8 Years of Age

Vuong

Braun

Sjödin

et al. 2016

Environ Health Perspect

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Background:Prenatal exposure to endocrine disruptors has been associated with increased risk of childhood obesity. However, epidemiologic studies on polybrominated diphenyl ethers (PBDEs) are limited despite animal studies indicating PBDEs’ potential role as an obesogen.Objectives:We investigated whether maternal concentrations of BDEs 28, 47, 99, 100, 153, and ΣPBDEs during pregnancy were associated with anthropometric measures in children aged 1–8 years.Methods:We examined 318 mother–child pairs in the Health Outcomes and Measures of the Environment (HOME) Study, a birth cohort enrolled from 2003 through 2006 (Cincinnati, OH). Serum PBDEs were measured at 16 ± 3 weeks gestation. We measured child height (1–8 years), weight (1–8 years), body mass index (BMI) (2–8 years), waist circumference (4–8 years), and body fat (8 years). To account for repeated measures, we used linear mixed models and generalized estimating equations to estimate associations between maternal PBDEs and child anthropometric measures.Results:We found no statistically significant associations between prenatal PBDEs and height or weight z-score. A 10-fold increase in maternal serum BDE-153 was associated with lower BMI z-score (β = –0.36; 95% CI: –0.60, –0.13) at 2–8 years, smaller waist circumference (β = –1.81 cm; 95% CI: –3.13, –0.50) at 4–8 years, and lower percent body fat (β = –2.37%; 95% CI: –4.21, –0.53) at 8 years. A decrease in waist circumference at 4–8 years was observed with a 10-fold increase in BDE-100 (β = –1.50 cm; 95% CI: –2.93, –0.08) and ΣPBDEs (β = –1.57 cm; 95% CI: –3.11, –0.02).Conclusions:Reverse causality may have resulted in prenatal PBDEs, particularly BDE-153, and decreased BMI, waist circumference, and body fat.Citation:Vuong AM, Braun JM, Sjödin A, Webster GM, Yolton K, Lanphear BP, Chen A. 2016. Prenatal polybrominated diphenyl ether exposure and body mass index in children up to 8 years of age. Environ Health Perspect 124:1891–1897; http://dx.doi.org/10.1289/EHP139

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Perinatal exposure to low-dose 2,2′,4,4′-tetrabromodiphenyl ether affects growth in rat offspring: What is the role of IGF-1?

Cited by 85 publications

References 48 publications

The Role of Epigenetics in the Latent Effects of Early Life Exposure to Obesogenic Endocrine Disrupting Chemicals

The Role of Epigenetics in the Latent Effects of Early Life Exposure to Obesogenic Endocrine Disrupting Chemicals

Adipose tissue accumulation of endocrine disrupting compounds: Variant of a common theme in exposome research

Prenatal Polybrominated Diphenyl Ether Exposure and Body Mass Index in Children Up To 8 Years of Age

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