Endocrine disrupting chemicals affect the adipogenic differentiation of mesenchymal stem cells in distinct ontogenetic windows

Biemann, Ronald; Santos, Anne Navarrete; Riemann, Dagmar; Knelangen, Julia M.; Blüher, Matthias; Koch, Holger M.; Fischer, Bernd

doi:10.1016/j.bbrc.2011.12.028

Cited by 69 publications

(58 citation statements)

References 38 publications

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“…Moreover, di(2-ethylhexyl) phthalate (DEHP) or its metabolite mono-(2-ethylhexyl) phthalate (MEHP) increased adipocyte differentiation in 3T3-L1 cells, (142) (115), murine mesenchymal stem cells (44), and in vivo (142) (62). Few human studies have addressed effects of BFRs on obesity and metabolic syndrome; however, adipocyte differentiation was increased by the BFRs PDBE (397) and BDE-47 (185).…”

Section: Effects Of Pops On At Functionmentioning

confidence: 99%

Adipose Tissue as a Site of Toxin Accumulation

Jackson

Shoemaker

Larian

et al. 2017

Comprehensive Physiology

136

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We examine the role of adipose tissue, typically considered an energy storage site, as a potential site of toxicant accumulation. Although the production of most persistent organic pollutants (POPs) was banned years ago, these toxicants persist in the environment due to their resistance to biodegradation and widespread distribution in various environmental forms (e.g., vapor, sediment, water). As a result, human exposure to these toxicants is inevitable. Largely due to their lipophilicity, POPs bioaccumulate in adipose tissue, resulting in greater body burdens of these environmental toxicants with obesity. POPs of major concern include polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins and furans (PCDDs/PCDFs), and polybrominated biphenyls and diphenyl ethers (PBBs/PBDEs), among other organic compounds. In this review, we 1) highlight the physical characteristics of toxicants that enable them to partition into and remain stored in adipose tissue, 2) discuss the specific mechanisms of action by which these toxicants act to influence adipocyte function, and 3) review associations between POP exposures and the development of obesity and diabetes. An area of controversy relates to the relative potential beneficial versus hazardous health effects of toxicant sequestration in adipose tissue.

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Section: Effects Of Pops On At Functionmentioning

confidence: 99%

Adipose Tissue as a Site of Toxin Accumulation

Jackson

Shoemaker

Larian

et al. 2017

Comprehensive Physiology

136

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“…Phthalates are known to induce the expression of PPAR gamma, modifying the expression of its target genes and the differentiation of these cells into adipocytes (Feige et al 2007; Hurst and Waxman 2003; Biemann et al 2012). The association between PPAR polymorphisms and obesity (Yao et al 2015; Redonnet et al 2002) may partly explain the larger associations observed in the right tail of first trimester BMI and early GWG, as the over-expression of PPAR gamma target genes induced by high levels of pregnancy phthalate exposure would more likely occur and have larger effects in those women with higher obesity levels before pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Urinary phthalate metabolite concentrations and maternal weight during early pregnancy

Bellavia

Hauser

Seely

et al. 2017

International Journal of Hygiene and Environmental Health

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Background Phthalates are a class of chemicals that may be associated with obesity in non-pregnant populations. Little is known about the association between pregnancy phthalate exposure and maternal obesity. Objective We evaluated the association between early-pregnancy urinary concentrations of specific phthalate metabolites and the distribution of body mass index (BMI, cross-sectional), and early gestational weight gain (GWG, prospective). Methods We measured 1st trimester urinary phthalate metabolite concentrations (median 9.9 weeks gestation) in 347 women from the LIFECODES pregnancy cohort (Boston, MA), who delivered term births. All measures were adjusted for specific-gravity and log-transformed. We used quantile regression to evaluate shifts in the entire outcome distributions, calculating multivariable-adjusted differences in the associations between these phthalate metabolites and BMI and GWG at the 25th, 50th, and 75th percentiles of these anthropometric outcomes. Results Higher concentrations of mono-ethyl phthalate (MEP) were associated with a rightward shift of 2.8 kg/m2 at the 75th percentiles of BMI (lowest vs highest quartile, 95% CI: 0.2–5.4) and 1.3 kg at the 75th percentiles of early GWG (lowest vs second quartiles, 95% CI: 0.3–2.4). A significant right-shift in the upper tail of BMI was also observed at higher concentrations of mono-benzyl (MBzP), mono-3-carboxypropyl (MCPP), and a summary measure of di-(2-ethylhexyl) phthalate metabolites (ΣDEHP). ΣDEHP was also associated with lower GWG. Conclusions Certain phthalates may be associated with shifts in maternal obesity measures, with MEP, MBzP, MCPP, and ΣDEHP being cross-sectionally associated with 1st trimester BMI and MEP and ΣDEHP being positively and inversely associated with early GWG, respectively.

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“…During the induction interval, BPA remained ineffective while TBT and DEHP increased the number of adipocytes, triglyceride content, and adipocyte-specific mRNA expression. Finally during terminal differentiation, only TBT promoted adipogenic differentiation while BPA or DEHP remained ineffective (Biemann et al 2011). This study demonstrated that EDCs can cooperate in a temporal manner to direct adipocyte differentiation.…”

Section: Developmental Programing Of Adipogenesis and Obesitymentioning

confidence: 67%

“…The ES cell-derived cardiac cell model was used to investigate xenoestrogen (Jung et al 2010) and dioxin (Wang et al 2010, Chatterjee et al 2013) activities in disrupting cardiomyocyte differentiation. Multipotent MSCs were used to study the underlying processes which regulate the developmental programing of adipogenesis and obesity , Kirchner et al 2010, Biemann et al 2011. Thus, embryonic cells exhibiting stem cell-like properties could be utilized to study the processes which are dysregulated by EDCs in utero and during early childhood.…”

Section: Discussionmentioning

confidence: 99%

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Actions of endocrine-disrupting chemicals on stem/progenitor cells during development and disease

Kopras

Potluri

Bermúdez

et al. 2013

Endocrine-Related Cancer

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Development and fate of the stem cell are regulated by extrinsic signals from the environment. Endocrine-disrupting chemicals which perturb hormonal signaling in utero and during early childhood may cause deregulation of multiple developmental processes, ranging from breakdown of stem cell niche architecture, developmental reprograming and altered stem cell fate to impaired organ and gonad development and sexual differentiation. Therefore, study of the environmental effects on stem cell integrity and normal development is a new and emerging focus for developmental biologists and cell toxicologists. When combined with new human and mouse stem cell-based models, stem cell differentiation dynamics can be studied in more biologically relevant ways. In this study, we review the current status of our understanding of the molecular mechanisms by which endocrine disruptors alter embryonic stem cell and adult stem/progenitor cell fate, organ development, cancer stem cell activity, and tumorigenesis.

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Endocrine disrupting chemicals affect the adipogenic differentiation of mesenchymal stem cells in distinct ontogenetic windows

Cited by 69 publications

References 38 publications

Adipose Tissue as a Site of Toxin Accumulation

Adipose Tissue as a Site of Toxin Accumulation

Urinary phthalate metabolite concentrations and maternal weight during early pregnancy

Actions of endocrine-disrupting chemicals on stem/progenitor cells during development and disease

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