Multigenerational study of the obesogen effects of bisphenol S after a perinatal exposure in C57BL6/J mice fed a high fat diet

Brulport, Axelle; Corre, Ludovic Le; Maquart, Guillaume; Barbet, Virginie; Dastugue, Aurélie; Séverin, Isabelle; Vaiman, Daniel; Chagnon, Marie‐Christine

doi:10.1016/j.envpol.2020.116243

Cited by 20 publications

(9 citation statements)

References 71 publications

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“…Results of this study show that early subchronic BPS exposure at 100 µg/kg/day for 10 weeks, in young mice led to a significant increase in body weight. These observations confirm previous evidence that BPS can be obesogenic (Brulport et al, 2021;Ivry Del Moral et al, 2016;Pu et al,2017;Thoene et al, 2020). Recently, it has been reported that perinatal BPS exposure induces sexdependent obesogenic multigenerational effects (Brulport et al, 2021).…”

Section: Discussionsupporting

confidence: 91%

“…These observations confirm previous evidence that BPS can be obesogenic (Brulport et al, 2021; Ivry Del Moral et al, 2016; Pu et al,2017; Thoene et al, 2020). Recently, it has been reported that perinatal BPS exposure induces sex‐dependent obesogenic multigenerational effects (Brulport et al, 2021). Such weight gain could be at least explained by an increase in energy intake (via an increase in food intake), while energy expenditures seem unaffected (at least the contribution of physical activity).…”

Section: Discussionsupporting

confidence: 91%

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Bisphenol S favors hepatic steatosis development via an upregulation of liver MCT1 expression and an impairment of the mitochondrial respiratory system

Mornagui

Rezg

Repond

et al. 2022

Journal Cellular Physiology

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Bisphenol S (BPS) is a common substitute of bisphenol A (BPA). Recent data suggest that BPS acts as an obesogenic endocrine disruptor with emerging implications in the physiopathology of metabolic syndrome. However, the effects of BPS on monocarboxylate transporters (acting as carriers for lactate, pyruvate, and ketone bodies) and the mitochondrial respiratory system in the liver remain limited. For this purpose, male Swiss mice were treated with BPS at 100 µg/kg/day for 10 weeks, in drinking water. An increase in body weight and food intake was observed with no increase in locomotor activity. Moreover, data show that BPS increases hepatic MCT1 (a key energetic fuel transporter) mRNA expression accompanied by hepatic steatosis initiation and lipid accumulation, while disrupting mitochondrial function and oxidative stress parameters. Furthermore, BPS produced a significant increase in lactate dehydrogenase and creatine kinase activities. We can suggest that BPS contributes to hepatic steatosis in mice by upregulating monocarboxylate transporters and affecting the bioenergetic status characterized by an impaired mitochondrial respiratory system. Thus, our data highlight a new mechanism putatively implicated in hepatic steatosis development during BPS‐induced obesity involving lactate metabolism.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 91%

Bisphenol S favors hepatic steatosis development via an upregulation of liver MCT1 expression and an impairment of the mitochondrial respiratory system

Mornagui

Rezg

Repond

et al. 2022

Journal Cellular Physiology

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“…Body weight was monitored weekly and body fat measured at euthanasia. Similar analyses were performed on the F2 and F3 generation offspring ( 131 ). Findings revealed interesting sex-dependent multigenerational effects, with multigenerational obesogenic effects found in both males and females, yet transgenerational effects only found in females, indicating that BPS is a likely sex-dependent obesogen.…”

Section: Bisphenolsmentioning

confidence: 93%

“…Both sexes showed a downregulation in genes involved in lipogenesis, however, only F2 females downregulated genes involved in lipolysis. The F3 generation showed striking sexual dimorphism in that increased visceral adipose tissue mass only occurred in females, as did the upregulation of genes involved in lipogenesis ( 131 ).…”

Section: Sexual Dimorphismsmentioning

confidence: 99%

Obesogens: How They Are Identified and Molecular Mechanisms Underlying Their Action

Mohajer

Checkcinco

et al. 2021

Front. Endocrinol.

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Adult and childhood obesity have reached pandemic level proportions. The idea that caloric excess and insufficient levels of physical activity leads to obesity is a commonly accepted answer for unwanted weight gain. This paradigm offers an inconclusive explanation as the world continually moves towards an unhealthier and heavier existence irrespective of energy balance. Endocrine disrupting chemicals (EDCs) are chemicals that resemble natural hormones and disrupt endocrine function by interfering with the body’s endogenous hormones. A subset of EDCs called obesogens have been found to cause metabolic disruptions such as increased fat storage, in vivo. Obesogens act on the metabolic system through multiple avenues and have been found to affect the homeostasis of a variety of systems such as the gut microbiome and adipose tissue functioning. Obesogenic compounds have been shown to cause metabolic disturbances later in life that can even pass into multiple future generations, post exposure. The rising rates of obesity and related metabolic disease are demanding increasing attention on chemical screening efforts and worldwide preventative strategies to keep the public and future generations safe. This review addresses the most current findings on known obesogens and their effects on the metabolic system, the mechanisms of action through which they act upon, and the screening efforts through which they were identified with. The interplay between obesogens, brown adipose tissue, and the gut microbiome are major topics that will be covered.

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“…F3 generation males showed no effects from ancestral BPS exposure while in females, VAT mass decreased and expression of lipogenic genes increased markedly. The authors suggested that DNA methylation, histone acetylation, and/or non-coding RNAs were likely avenues of transgenerational inheritance, although these avenues were not explored in the study ( 22 ).…”

Section: Transgenerational Inheritance Of Obesitymentioning

confidence: 99%

Epigenetic Transgenerational Inheritance of the Effects of Obesogen Exposure

et al. 2021

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Obesity and metabolic disorders have become a worldwide pandemic affecting millions of people. Although obesity is a multifaceted disease, there is growing evidence supporting the obesogen hypothesis, which proposes that exposure to a subset of endocrine disrupting chemicals (EDCs), known as obesogens, promotes obesity. While these effects can be observed in vitro using cell models, in vivo and human epidemiological studies have strengthened this hypothesis. Evidence from animal models showed that the effects of obesogen exposure can be inherited transgenerationally through at least the F4 generation. Transgenerational effects of EDC exposure predispose future generations to undesirable phenotypic traits and diseases, including obesity and related metabolic disorders. The exact mechanisms through which phenotypic traits are passed from an exposed organism to their offspring, without altering the primary DNA sequence, remain largely unknown. Recent research has provided strong evidence suggesting that a variety of epigenetic mechanisms may underlie transgenerational inheritance. These include differential DNA methylation, histone methylation, histone retention, the expression and/or deposition of non-coding RNAs and large-scale alterations in chromatin structure and organization. This review highlights the most recent advances in the field of epigenetics with respect to the transgenerational effects of environmental obesogens. We highlight throughout the paper the strengths and weaknesses of the evidence for proposed mechanisms underlying transgenerational inheritance and why none of these is sufficient to fully explain the phenomenon. We propose that changes in higher order chromatin organization and structure may be a plausible explanation for how some disease predispositions are heritable through multiple generations, including those that were not exposed. A solid understanding of these possible mechanisms is essential to fully understanding how environmental exposures can lead to inherited susceptibility to diseases such as obesity.

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Multigenerational study of the obesogen effects of bisphenol S after a perinatal exposure in C57BL6/J mice fed a high fat diet

Cited by 20 publications

References 71 publications

Bisphenol S favors hepatic steatosis development via an upregulation of liver MCT1 expression and an impairment of the mitochondrial respiratory system

Bisphenol S favors hepatic steatosis development via an upregulation of liver MCT1 expression and an impairment of the mitochondrial respiratory system

Obesogens: How They Are Identified and Molecular Mechanisms Underlying Their Action

Epigenetic Transgenerational Inheritance of the Effects of Obesogen Exposure

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