The environmental obesogen bisphenol A increases macrophage self-renewal

Ampem, Grace; Junginger, Alexandra; Yu, Haidong; Thuróczy, Julianna; Schneider, Marion; Röszer, Tamás

doi:10.1007/s00441-019-03019-5

Cited by 10 publications

(6 citation statements)

References 96 publications

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“…Additionally, mice exposed to BPA perinatally showed increased presence of macrophages in gonadal white adipose tissue [86]. BPA has also been shown to increase macrophage self-renewal [87]. BPA is one of the most widely studied obesogens but it is likely that an influx of inflammatory cells plays a role in other obesogens as well.…”

Section: Inflammationmentioning

confidence: 99%

Mechanisms of action, chemical characteristics, and model systems of obesogens

et al. 2020

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There is increasing evidence for the role of environmental endocrine disrupting contaminants, coined obesogens, in exacerbating the rising obesity epidemic. Obesogens can be found in everyday items ranging from pesticides to food packaging. Although research shows that obesogens can have effects on adipocyte size, phenotype, metabolic activity, and hormone levels, much remains unknown about these chemicals. This review will discuss what is currently known about the mechanisms of obesogens, including expression of the PPARs, hormone interference, and inflammation. Strategies for identifying obesogenic chemicals and their mechanisms through chemical characteristics and model systems will also be discussed. Ultimately, research should focus on improving models to discern precise mechanisms of obesogenic action and to test therapeutics targeting these mechanisms.

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Section: Inflammationmentioning

confidence: 99%

Mechanisms of action, chemical characteristics, and model systems of obesogens

et al. 2020

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“…In contrast, M2 subtype has the characteristic of relatively high expression of surface marker CD206 and production of arginase (Arg-1) and anti-inflammatory cytokines such as transforming growth factor (TGF)-β and IL-10 (Martinez et al, 2009;Sica and Marques, 2012;Murray et al, 2014). Numerous studies have demonstrated BPA exposure-induced downregulation of macrophage activity, decrease in macrophages phagocytic function and influence of inflammatory responses via modulating the cytokine expression of macrophages (Ampem et al, 2019;Berntsen et al, 2018;Li et al, 2018aLi et al, , 2018bTeixeria et al, 2016;Liu et al, 2014;Pyo et al, 2007;Byun et al, 2005). However, the effects of BPA exposure on macrophage polarization and the underlying molecular mechanisms remain largely undefined.…”

Section: Introductionmentioning

confidence: 99%

Bisphenol A promotes macrophage proinflammatory subtype polarization via upregulation of IRF5 expression in vitro

et al. 2019

Toxicology in Vitro

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“…The metaflammation (low-grade chronic adipose tissue inflammation) is consistently associated with excess body fats, adiposity, hyper corticosterone, and expression of proinflammatory cytokines observed in BPS-exposed offspring, indicating severely inflamed adipose tissue. The macrophage numbers might have elevated in bisphenol-exposed adipose tissues as their increased accumulation activated the pro-inflammatory cascade (Ampem et al, 2019). BPS-exposed rats become obese due to severe metabolic and systemic inflammation impairment propelled by macrophage accumulation (Weisberg et al, 2003), as evidenced by upregulated IL1β, CRP, and COX2 expression in our study.…”

Section: Discussionmentioning

confidence: 55%

Gestational exposure to bisphenol S induces microvesicular steatosis by promoting lipogenesis and inflammation in male rat offspring

Molangiri,

Varma,

Hridayanka

et al. 2023

Preprint

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Fetal exposure to endocrine-disrupting bisphenol A (BPA) showed a long-lasting programming effect on organ development and predisposed to the metabolic risk of adult diseases. However, limited data on developmental exposure to BPA-substitute bisphenol S (BPS) in predisposing liver metabolic disease is available. Here, the effects of BPS exposure were assessed on hepatic metabolism by examining adiposity and inflammation in the adipose and liver of the 90-day male offspring. Pregnant Wistar rats were exposed to BPA and BPS (0.0, 0.4, 4.0 microgram/kg bw) via gavage from gestational day 4 to 21. Prenatal BPS-exposed offspring exhibited a higher obesogenic effect than BPA, including changes in body weight, body fat, feed efficiency, and leptin signalling. The fasting blood glucose did not change, but BPS exposure elevated plasma corticosterone levels and adipocyte hypertrophy of the visceral adipose tissue (VAT) to a greater extent than BPA. Adipocyte hypertrophy was augmented by modulated expression of lipid uptake (PPARgamma, FABP4), glucocorticoid (HSD11 beta1), inflammation (IL6, IL1beta, CRP, COX2), oxidative stress (CHOP) and apoptotic (Caspase 3) mediators. Liver histology showed numerous lipid droplets, and hepatocyte ballooning, associated with upregulated expression of cholesterol, lipid biogenesis and glucocorticoid activators, indicating microvesicular steatosis in the prenatally BPS-exposed adult offspring. The upregulated PPARalpha, ADRP, and FGF21 expression and increased lipid peroxidation in the offspring's liver suggest metaflammation due to fetal exposure to BPS. Fetal BPS exposure demonstrated a more significant disruption in metabolism involving adiposity, liver fat, inflammation in excess, and predisposition to hepatic steatosis in the male offspring.

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The environmental obesogen bisphenol A increases macrophage self-renewal

Cited by 10 publications

References 96 publications

Mechanisms of action, chemical characteristics, and model systems of obesogens

Mechanisms of action, chemical characteristics, and model systems of obesogens

Bisphenol A promotes macrophage proinflammatory subtype polarization via upregulation of IRF5 expression in vitro

Gestational exposure to bisphenol S induces microvesicular steatosis by promoting lipogenesis and inflammation in male rat offspring

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