Effects of Bisphenol S on hypothalamic neuropeptides regulating feeding behavior and apelin/APJ system in mice

Rezg, Raja; Abot, Anne; Mornagui, Bessem; Aydi, Samir; Knauf, Claude

doi:10.1016/j.ecoenv.2018.06.001

Cited by 40 publications

(29 citation statements)

References 44 publications

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“…No other maternal OPFR studies has characterized feeding behaviors in rodents, whether on LFD or HFD (Baldwin et al, 2017; Patisaul et al, 2013; Wang et al, 2018; Wang et al, 2019). In terms of other EDCs, a replacement compound for BPA, bisphenol S, also increased Agrp with no change in Pomc , Npy or Cart , in male mice (no females examined) (Rezg, Abot, Mornagui, Aydi, & Knauf, 2018). In comparison, perinatal BPA‐exposed mice had a reduction in Pomc with no change in Agrp , while in another study, BPA increased Pomc potentially through a PPARγ‐mediated mechanism (MacKay, Patterson, & Abizaid, 2017; Salehi, Loganathan, & Belsham, 2019).…”

Section: Discussionmentioning

confidence: 99%

Maternal organophosphate flame‐retardant exposure alters offspring feeding, locomotor and exploratory behaviors in a sexually‐dimorphic manner in mice

Walley

Krumm

Yasrebi

et al. 2020

J of Applied Toxicology

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Increased usage of organophosphate flame retardants (OPFRs) has led to detectable levels in pregnant women and neonates, which is associated with negative neurological outcomes. Therefore, we investigated if maternal OPFR exposure altered adult offspring feeding, locomotor, and anxiety‐like behaviors on a low‐fat (LFD) or high‐fat diet (HFD). Wild‐type C57Bl/6J dams were orally dosed with vehicle (sesame oil) or an OPFR mixture (1 mg/kg combination each of tris(1,3‐dichloro‐2‐propyl)phosphate, triphenyl phosphate and tricresyl phosphate) from gestation day 7 to postnatal day 14. After weaning, pups were fed either a LFD or HFD until 19 weeks of age. Locomotor and anxiety‐like behaviors were evaluated with the open field test, elevated plus maze, and metabolic cages. Feeding behaviors and meal patterns were analyzed by a Biological Data Acquisition System. Anogenital distance was reduced in OPFR‐exposed male pups, but no effect was detected on adult body weight. We observed interactions of OPFR exposure and HFD consumption on locomotor and anxiety‐like behavior in males, suggesting an anxiogenic effect while reducing overall nighttime activity. We also observed an interaction of OPFR exposure and HFD on weekly food intake and feeding behaviors. OPFR‐exposed males consumed more total HFD than oil‐exposed males during the 72‐hour trial. However, when arcuate gene expression was analyzed, OPFR exposure induced Agrp expression in females, which would suggest greater orexigenic tone. Collectively, the implications of our study are that the behavioral effects of OPFR exposure are modulated by adult HFD consumption, which may influence the metabolic and neurological consequences of maternal OPFR exposure.

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Section: Discussionmentioning

confidence: 99%

Maternal organophosphate flame‐retardant exposure alters offspring feeding, locomotor and exploratory behaviors in a sexually‐dimorphic manner in mice

Walley

Krumm

Yasrebi

et al. 2020

J of Applied Toxicology

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“…In vivo, perinatal exposure to low BPA doses affected the structural and functional developmental programming of POMC circuitry in male and female mice [187]. Conversely, administration of BPS (25, 50, 100 µg/kg) in drinking water after weaning for 10 weeks altered the orexygenic AgRP neuropeptide but not the anorexygenic neuropeptides POMC and CART [188]. Also, the main endocannabinoid, anandamide (AEA), a lipid derivative of the arachydonic acid which activates type1 cannabinoid receptor (CB1), has a recognized role in the hypothalamic control of food intake and reproduction.…”

Section: Bpa Interference In Energy Intake and Reproductionmentioning

confidence: 95%

Neuro-toxic and Reproductive Effects of BPA

et al. 2019

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Background: Bisphenol A (BPA) is one of the highest volume chemicals produced worldwide. It has recognized activity as an endocrine-disrupting chemical and has suspected roles as a neurological and reproductive toxicant. It interferes in steroid signaling, induces oxidative stress, and affects gene expression epigenetically. Gestational, perinatal and neonatal exposures to BPA affect developmental processes, including brain development and gametogenesis, with consequences on brain functions, behavior, and fertility. Methods: This review critically analyzes recent findings on the neuro-toxic and reproductive effects of BPA (and its analogues), with focus on neuronal differentiation, synaptic plasticity, glia and microglia activity, cognitive functions, and the central and local control of reproduction. Results: BPA has potential human health hazard associated with gestational, peri- and neonatal exposure. Beginning with BPA’s disposition, this review summarizes recent findings on the neurotoxicity of BPA and its analogues, on neuronal differentiation, synaptic plasticity, neuroinflammation, neuro-degeneration, and impairment of cognitive abilities. Furthermore, it reports the recent findings on the activity of BPA along the HPG axis, effects on the hypothalamic Gonadotropin Releasing Hormone (GnRH), and the associated effects on reproduction in both sexes and successful pregnancy. Conclusion: BPA and its analogues impair neuronal activity, HPG axis function, reproduction, and fertility. Contrasting results have emerged in animal models and human. Thus, further studies are needed to better define their safety levels. This review offers new insights on these issues with the aim to find the “fil rouge”, if any, that characterize BPA’s mechanism of action with outcomes on neuronal function and reproduction.

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“…While studies on BPA effects are slowly increasing, only a few studies focus on BPA-analogs: postnatal exposure from PND21 for 10 weeks with 25-50-100 μg/kg BW/day of bisphenol S (BPS) in drinking water affects orexigenic hypothalamic systems resulting in a dose-dependent increase of AgRP mRNA level but not in NPY one or in anorexigenic neuropeptides [POMC, CART; (24)].…”

Section: Central Action Of Metabolism-disrupting Chemicals (Mdcs)mentioning

confidence: 99%

Metabolism Disrupting Chemicals and Alteration of Neuroendocrine Circuits Controlling Food Intake and Energy Metabolism

et al. 2019

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The metabolism-disrupting chemicals (MDCs) are molecules (largely belonging to the category of endocrine disrupting chemicals, EDCs) that can cause important diseases as the metabolic syndrome, obesity, Type 2 Diabetes Mellitus or fatty liver. MDCs act on fat tissue and liver, may regulate gut functions (influencing absorption), but they may also alter the hypothalamic peptidergic circuits that control food intake and energy metabolism. These circuits are normally regulated by several factors, including estrogens, therefore those EDCs that are able to bind estrogen receptors may promote metabolic changes through their action on the same hypothalamic circuits. Here, we discuss data showing how the exposure to some MDCs can alter the expression of neuropeptides within the hypothalamic circuits involved in food intake and energy metabolism. In particular, in this review we have described the effects at hypothalamic level of three known EDCs: Genistein, an isoflavone (phytoestrogen) abundant in soy-based food (a possible new not-synthetic MDC), Bisphenol A (compound involved in the manufacturing of many consumer plastic products), and Tributyltin chloride (one of the most dangerous and toxic endocrine disruptor, used in antifouling paint for boats).

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Effects of Bisphenol S on hypothalamic neuropeptides regulating feeding behavior and apelin/APJ system in mice

Cited by 40 publications

References 44 publications

Maternal organophosphate flame‐retardant exposure alters offspring feeding, locomotor and exploratory behaviors in a sexually‐dimorphic manner in mice

Maternal organophosphate flame‐retardant exposure alters offspring feeding, locomotor and exploratory behaviors in a sexually‐dimorphic manner in mice

Neuro-toxic and Reproductive Effects of BPA

Metabolism Disrupting Chemicals and Alteration of Neuroendocrine Circuits Controlling Food Intake and Energy Metabolism

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