Estrogenic chemicals at body burden levels attenuate energy metabolism in 3T3‐L1 adipocytes

Tsou, Tsui‐Chun; Yeh, Szu-Ching; Hsu, Jhih-Wei; Tsai, Feng-Yuan

doi:10.1002/jat.3508

Cited by 8 publications

(6 citation statements)

References 32 publications

(38 reference statements)

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“…ages STAT1 function to amplify inflammatory responses and disrupt mitochondrial function. Other EDCs including BPA (3,9,13,16,65,66), BPA analogs (7,8), and tributyltin (59) likely also leverage proinflammatory pathways to induce mitochondrial dysfunction in adipocytes. A prominent effect of chronic interferon activation in adipocytes is reduced mitochondrial function and morphology (31,34).…”

Section: Discussionmentioning

confidence: 99%

Bisphenol AF promotes inflammation in human white adipocytes

Chernis

Masschelin

Cox

et al. 2020

American Journal of Physiology-Cell Physiology

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Endocrine-disrupting chemicals interact with transcription factors essential for adipocyte differentiation. Exposure to endocrine-disrupting chemicals corresponds with elevated risks of obesity, but the effects of these compounds on human cells remain largely undefined. Widespread use of bisphenol AF (BPAF) as a bisphenol A (BPA) alternative in the plastics industry presents unknown health risks. To this end, we discovered that BPAF interferes with the metabolic function of mature human adipocytes. Although 4-day exposures to BPAF accelerated adipocyte differentiation, we observed no effect on mature fat cell marker genes. Additional gene and protein expression analysis showed that BPAF treatment during human adipocyte differentiation failed to suppress the proinflammatory transcription factor STAT1. Microscopy and respirometry experiments demonstrated that BPAF impaired mitochondrial function and structure. To test the hypothesis that BPAF fosters vulnerabilities to STAT1 activation, we treated mature adipocytes previously exposed to BPAF with interferon-γ (IFNγ). BPAF increased IFNγ activation of STAT1 and exposed mitochondrial vulnerabilities that disrupt adipocyte lipid and carbohydrate metabolism. Collectively, our data establish that BPAF activates inflammatory signaling pathways that degrade metabolic activity in human adipocytes. These findings suggest how the BPA alternative BPAF contributes to metabolic changes that correspond with obesity.

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Section: Discussionmentioning

confidence: 99%

Bisphenol AF promotes inflammation in human white adipocytes

Chernis

Masschelin

Cox

et al. 2020

American Journal of Physiology-Cell Physiology

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“…In human adipose-derived stem cells, tributyltin (100 nM) inhibited oxygen consumption (Llobet et al 2015). Similarly, 3T3-L1 adipocytes exposed to BPA (10 nM), 4-nonylphenol (600 pM) and diethylstilbestrol (0.23 pM) exhibited decreased mitochondrial respiration and mitochondria-associated ATP production, as well as reduced glycolytic function (Tsou et al 2017). These effects might be due to direct effects on the activity of mitochondrial proteins and/or modulation of mitochondria biogenesis, which are consistent with the mitochondrial impairment observed in WAT from obese/ T2D individuals (Bogacka et al 2005, Choo et al 2006, Dahlman et al 2006, Rong et al 2007.…”

Section: Journal Of Endocrinologymentioning

confidence: 98%

Mitochondria as target of endocrine-disrupting chemicals: implications for type 2 diabetes

Marroquí

Tudurí

Alonso-Magdalena

et al. 2018

Journal of Endocrinology

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Type 2 diabetes is a chronic, heterogeneous syndrome characterized by insulin resistance and pancreatic β-cell dysfunction or death. Among several environmental factors contributing to type 2 diabetes development, endocrine-disrupting chemicals (EDCs) have been receiving special attention. These chemicals include a wide variety of pollutants, from components of plastic to pesticides, with the ability to modulate endocrine system function. EDCs can affect multiple cellular processes, including some related to energy production and utilization, leading to alterations in energy homeostasis. Mitochondria are primarily implicated in cellular energy conversion, although they also participate in other processes, such as hormone secretion and apoptosis. In fact, due to mitochondria involvement in so many crucial cellular processes in metabolic relevant tissues, mitochondrial dysfunction has been linked to different metabolic diseases, including insulin resistance and type 2 diabetes. Herein, we review the main mechanisms whereby metabolism-disrupting chemical (MDC), a subclass of EDCs that disturbs energy homeostasis, cause mitochondrial dysfunction, thus contributing to the establishment of insulin resistance and type 2 diabetes. We conclude that MDC-induced mitochondrial dysfunction, which is mainly characterized by perturbations in mitochondrial bioenergetics, biogenesis, and dynamics, excessive reactive oxygen species production, and activation of the mitochondrial pathway of apoptosis, seems to be a relevant mechanism linking MDCs to type 2 diabetes development.

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“…Prenatal exposure to BPA (50 μg/kg/day) downregulated Cyt-C expression in heart tissue of neonatal rats (Marroqui et al 2018). 3T3-L1 adipocytes treated with BPA (10 nM), nonylphenol (600 pM), and diethylstilbestrol (0.23 pM) displayed reduced respiration, ATP production and glycolytic functions (Tsou et al 2017). BPA-induced impaired mitochondrial bioenergetics may contribute to hepatotoxicity.…”

Section: Bioenergetics and Respirationmentioning

confidence: 96%

Impact of Bisphenol A on Structure and Function of Mitochondria: A Critical Review

Nayak

Adiga

Khan

et al. 2022

Reviews Env.Contamination (formerly:Residue Reviews)

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Bisphenol A (BPA) is an industrial chemical used extensively to manufacture polycarbonate plastics and epoxy resins. Because of its estrogen-mimicking properties, BPA acts as an endocrine-disrupting chemical. It has gained attention due to its high chances of daily and constant human exposure, bioaccumulation, and the ability to cause cellular toxicities and diseases at extremely low doses. Several elegant studies have shown that BPA can exert cellular toxicities by interfering with the structure and function of mitochondria, leading to mitochondrial dysfunction. Exposure to BPA results in oxidative stress and alterations in mitochondrial DNA (mtDNA), mitochondrial biogenesis, bioenergetics, mitochondrial membrane potential (MMP) decline, mitophagy, and apoptosis. Accumulation of reactive oxygen species (ROS) in conjunction with oxidative damage may be responsible for causing BPA-mediated cellular toxicity. Thus, several reports have suggested using antioxidant treatment to mitigate the toxicological effects of BPA. The present literature review emphasizes the adverse effects of BPA on mitochondria, with a comprehensive note on the molecular aspects of the structural and functional alterations in mitochondria in response to BPA exposure. The review also confers the possible approaches to alleviate BPA-mediated oxidative damage and the existing knowledge gaps in this emerging area of research.

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Estrogenic chemicals at body burden levels attenuate energy metabolism in 3T3‐L1 adipocytes

Cited by 8 publications

References 32 publications

Bisphenol AF promotes inflammation in human white adipocytes

Bisphenol AF promotes inflammation in human white adipocytes

Mitochondria as target of endocrine-disrupting chemicals: implications for type 2 diabetes

Impact of Bisphenol A on Structure and Function of Mitochondria: A Critical Review

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