Chronic exposure of mice to environmental endocrine-disrupting chemicals disturbs their energy metabolism

Jin, Yuanxiang; Lin, Xiaojian; Miao, Wenyu; Wu, Tao; Shen, Hangjie; Chen, Shan; Li, Yanhong; Pan, Qiaoqiao; Fu, Zhengwei

doi:10.1016/j.toxlet.2014.01.006

Cited by 51 publications

(36 citation statements)

References 50 publications

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“…1B, the liver in the CON group did not show any significant changes after the experiment; in contrast, obvious lipid accumulation was observed in the liver of the HD group, and this fat accumulation was clearly ameliorated by the administration with IOE for 12 weeks. To confirm this observation, the contents of hepatic TG and TC were further examined as previously described [9]. The hepatic TG and TC levels in the HD group were significantly higher than those in the CON group (Fig.…”

mentioning

confidence: 62%

Ameliorating effects of <italic>Inonotus obliquus</italic> on high fat diet-induced obese rats

Wu¹,

Shu²,

Yang³

et al. 2015

ABBS

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confidence: 62%

Ameliorating effects of <italic>Inonotus obliquus</italic> on high fat diet-induced obese rats

Wu¹,

Shu²,

Yang³

et al. 2015

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“…Metabolic disruption has been previously demonstrated for some of these chemicals in vivo , including FM550 and several components 42 , permethrin 43 and cypermethrin 44 , and DEHP 45 . Some of these chemicals have been previously assessed in 3T3-L1 cells, and agree with our results.…”

Section: Discussionmentioning

confidence: 90%

Characterization of Adipogenic Activity of House Dust Extracts and Semi-Volatile Indoor Contaminants in 3T3-L1 Cells

Kassotis

Hoffman

Stapleton

2017

Environ. Sci. Technol.

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Obesity and metabolic disorders are of great societal concern and generate significant human health care costs. Recently, attention has focused on the potential for environmental contaminants to act as metabolic disruptors. This study sought to evaluate the adipogenic activity of indoor house dust extracts and a suite of semi-volatile organic chemicals (SVOCs) that are often ubiquitously detected in indoor environments. 3T3-L1 cells were exposed to extracts of indoor dust or individual SVOCs and assessed for triglyceride accumulation and pre-adipocyte proliferation. Ten of 11 house dust extracts exhibited significant triglyceride accumulation and/or proliferation at environmentally relevant levels (<20 μg of dust/well), and significant adipogenic activity was also exhibited by 28 of the SVOCs. Notably, pyraclostrobin, dibutyl phthalate, tert-butyl-phenyl diphenyl phosphate, and the isopropylated triaryl phosphates (ITPs) exhibited near maximal or supra-maximal triglyceride accumulation relative to the rosiglitazone-induced maximum. The adipogenic activity in house dust occurred at concentrations below EPA estimated child exposure levels, and raises concerns for human health impacts, particularly in children. Our results delineate a novel potential health threat and identify putative causative SVOCs that are likely contributing to this activity.

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“…In addition to BPA, other EDCs can enhance NAFLD when promoted by a HFD (for example, treatment of mice with PFOA 108 or the pesticides CYP or ATZ 109 ). Importantly, some EDC exposures alone failed to trigger disease, with NAFLD observed only when EDC exposure was combined with a HFD.…”

Section: Liver Fat Metabolism and Edcsmentioning

confidence: 99%

Endocrine-disrupting chemicals and fatty liver disease

et al. 2017

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Nonalcoholic fatty liver disease (NAFLD) is a growing epidemic paralleling the increase in obesity and diabetes mellitus seen in Western diet-consuming countries. As NAFLD can lead to life-threatening conditions such as cirrhosis and hepatocellular carcinoma (HCC), an understanding of factors that trigger its development and pathological progression is needed. Although by definition this disease is not associated with alcohol consumption, exposure to environmental agents that have been linked to other diseases might have a role in the development of NAFLD. Here, we focus on one class of these agents, endocrine-disrupting chemicals (EDCs), and their potential to influence the initiation and progression of a cascade of pathological conditions associated with fatty liver. Experimental studies have revealed several potential mechanisms by which EDC exposures might contribute to disease pathogenesis, including modulation of nuclear hormone receptor (NR) function and alteration of the epigenome. However, many questions remain to be addressed about the causal link between acute and chronic EDC exposure and the development of NAFLD in humans. Future studies that address these questions hold promise not only for understanding the linkage between EDC exposure and liver disease, but for elucidating the molecular mechanisms underpinning NAFLD and the development of new prevention and treatment opportunities.

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Chronic exposure of mice to environmental endocrine-disrupting chemicals disturbs their energy metabolism

Cited by 51 publications

References 50 publications

Ameliorating effects of <italic>Inonotus obliquus</italic> on high fat diet-induced obese rats

Ameliorating effects of <italic>Inonotus obliquus</italic> on high fat diet-induced obese rats

Characterization of Adipogenic Activity of House Dust Extracts and Semi-Volatile Indoor Contaminants in 3T3-L1 Cells

Endocrine-disrupting chemicals and fatty liver disease

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Chronic exposure of mice to environmental endocrine-disrupting chemicals disturbs their energy metabolism

Cited by 51 publications

References 50 publications

Ameliorating effects of &lt;italic&gt;Inonotus obliquus&lt;/italic&gt; on high fat diet-induced obese rats

Ameliorating effects of &lt;italic&gt;Inonotus obliquus&lt;/italic&gt; on high fat diet-induced obese rats

Characterization of Adipogenic Activity of House Dust Extracts and Semi-Volatile Indoor Contaminants in 3T3-L1 Cells

Endocrine-disrupting chemicals and fatty liver disease

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Product

Resources

About

Ameliorating effects of <italic>Inonotus obliquus</italic> on high fat diet-induced obese rats

Ameliorating effects of <italic>Inonotus obliquus</italic> on high fat diet-induced obese rats