The environmental obesogen bisphenol A promotes adipogenesis by increasing the amount of 11β-hydroxysteroid dehydrogenase type 1 in the adipose tissue of children

Wang, Jinfan; Sun, Bin; Hou, Meng; Pan, Xiaoqing; Li, X

doi:10.1038/ijo.2012.173

Cited by 114 publications

(83 citation statements)

References 40 publications

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“…Data are presented as mean ± SEM of five independent experiments using five different placentas ( * p < 0.05, ** p < 0.01, *** p < 0.001 vs. control). potential adverse effects [3], coupled with the recent findings that BPA stimulates 11␤-HSD1 activity and expression in adipocytes isolated from visceral adipose tissue of children [32], we hypothesized that BPA regulates human placental 11␤-HSD2. To test this hypothesis, we utilized our established primary human trophoblast cells as an in vitro model system.…”

Section: Discussionmentioning

confidence: 97%

Bisphenol A disrupts gene expression in human placental trophoblast cells

Rajakumar

Guan

Langlois

et al. 2015

Reproductive Toxicology

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Section: Discussionmentioning

confidence: 97%

Bisphenol A disrupts gene expression in human placental trophoblast cells

Rajakumar

Guan

Langlois

et al. 2015

Reproductive Toxicology

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“…Several EDCs have been shown to upregulate MSC and preadipocyte differentiation into adipocytes at concentrations ranging from 100 pM to 100 μM: dichlorodiphenyltrichloroethane or 1,1,1-trichloro-2,2-bis ( p -chlorophenyl)-ethane (DDT), 4-nonylphenol (4-NP), octylphenol (OP), bisphenol A (BPA), polychlorinated biphenyl (PCB)-77, PCB-101, PCB-153, PCB-180, di-(2-ethyl hexyl)phthalate (DEHP), mono-(2-ethylhexyl)phthalate (MEHP), dibutyl phthalate (DBP), benzyl butyl phthalate (BBP), dicyclohexyl phthalate (DCHP), and mono-benzyl phthalate (MBzP) (30, 35, 37, 39, 40, 42, 43, 46, 63, 66–80). Many endocrine disruptors target PPARγ by binding to it directly to activate downstream cascades that lead to enhanced adipogenesis or by increasing PPARγ expression to allow for a lower threshold for activation.…”

Section: Adipogenesismentioning

confidence: 99%

The Effects of Endocrine Disruptors on Adipogenesis and Osteogenesis in Mesenchymal Stem Cells: A Review

et al. 2017

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Endocrine-disrupting chemicals (EDCs) are prevalent in the environment, and epidemiologic studies have suggested that human exposure is linked to chronic diseases, such as obesity and diabetes. In vitro experiments have further demonstrated that EDCs promote changes in mesenchymal stem cells (MSCs), leading to increases in adipogenic differentiation, decreases in osteogenic differentiation, activation of pro-inflammatory cytokines, increases in oxidative stress, and epigenetic changes. Studies have also shown alteration in trophic factor production, differentiation ability, and immunomodulatory capacity of MSCs, which have significant implications to the current studies exploring MSCs for tissue engineering and regenerative medicine applications and the treatment of inflammatory conditions. Thus, the consideration of the effects of EDCs on MSCs is vital when determining potential therapeutic uses of MSCs, as increased exposure to EDCs may cause MSCs to be less effective therapeutically. This review focuses on the adipogenic and osteogenic differentiation effects of EDCs as these are most relevant to the therapeutic uses of MSCs in tissue engineering, regenerative medicine, and inflammatory conditions. This review will highlight the effects of EDCs, including organophosphates, plasticizers, industrial surfactants, coolants, and lubricants, on MSC biology.

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“…The adipogenic effect of BPA has been proposed to be mediated by an ER-dependent mechanism, along with the enhanced expression of DLK (leucine zipper-bearing kinase), insulin-like growth factor-1 (IGF-1), C/EBPα, or PPARγ among other factors [14,55]. Furthermore, BPA has been reported to promote the adipogenesis by increasing expression and enzyme activity of 11β-hydroxysteroid dehydrogenase type 1 [56], the thyroid receptor/retinoic X receptor or mammalian target of rapamycin signaling pathways [57]. Previous in vivo studies have demonstrated that the prenatal BPA exposure is linked to DNA methylation variation of Insulin-like Growth Factor 2 (IGF-2) and H19, two reciprocally expressed imprinted genes located on chromosome 11p15.5 that play a major role in fetal and placental growth [29].…”

Section: Bisphenol Amentioning

confidence: 99%

Endocrine Aspects of Environmental “Obesogen” Pollutants

Nappi

Barrea

Somma

et al. 2016

IJERPH

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Growing evidence suggests the causal link between the endocrine-disrupting chemicals (EDCs) and the global obesity epidemics, in the context in the so-called “obesogenic environment”. Dietary intake of contaminated foods and water, especially in association with unhealthy eating pattern, and inhalation of airborne pollutants represent the major sources of human exposure to EDCs. This is of particular concern in view of the potential impact of obesity on chronic non-transmissible diseases, such as type 2 diabetes, cardiovascular disease, and hormone-sensitive cancers. The key concept is the identification of adipose tissue not only as a preferential site of storage of EDCs, but also as an endocrine organ and, as such, susceptible to endocrine disruption. The timing of exposure to EDCs is critical to the outcome of that exposure, with early lifetime exposures (e.g., fetal or early postnatal) particularly detrimental because of their permanent effects on obesity later in life. Despite that the mechanisms operating in EDCs effects might vary enormously, this minireview is aimed to provide a general overview on the possible association between the pandemics of obesity and EDCs, briefly describing the endocrine mechanisms linking EDCs exposure and latent onset of obesity.

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The environmental obesogen bisphenol A promotes adipogenesis by increasing the amount of 11β-hydroxysteroid dehydrogenase type 1 in the adipose tissue of children

Abstract: BPA, at environmentally relevant levels, increased the mRNA expression and enzymatic activity of 11β-HSD1 by acting upon a GC receptor, which may lead to the acceleration of adipogenesis.

Cited by 114 publications

References 40 publications

Bisphenol A disrupts gene expression in human placental trophoblast cells

Bisphenol A disrupts gene expression in human placental trophoblast cells

The Effects of Endocrine Disruptors on Adipogenesis and Osteogenesis in Mesenchymal Stem Cells: A Review

Endocrine Aspects of Environmental “Obesogen” Pollutants

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