Co-exposure to endocrine disruptors: effect of bisphenol A and soy extract on glucose homeostasis and related metabolic disorders in male mice

Veissi, Masoud; Jafarirad, Sima; Ahangarpour, Akram; Mohaghegh, Seyede Marjan; Malehi, Amal Saki

doi:10.2478/enr-2018-0009

Cited by 9 publications

(7 citation statements)

References 46 publications

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“…(28,29) Given their deregulatory properties, EDCs may impact glycoregulatory hormones. (30) Pre and postnatal exposure to glyphosate (Roundup Original DI  ) increased glucose sensitivity in the GBH-F1 Group on PND60 in this study. Although this parameter was normalized by PND143, glucose level decline after insulin administration was significantly higher in the GBH-F1 compared to the CTRL-F1 Group, suggesting higher sensitivity to this hormone.…”

Section: Liver Histology In Male F1 Offspringmentioning

confidence: 48%

“…Tizhe et al (31) reported a subtle (non-significant) increase in plasma glucose and insulin levels in male rats exposed to different concentrations of Bushfire  (a commercial formulation of glyphosate). Veissi et al (30) observed increased glycemia and decreased insulinemia in male mice exposed to Bisphenol A (BPA) (diphenol used in plastic products, with endocrine disrupting effects). According to Bonvallot et al (32) exposure to a mixture of eight pesticides commonly found in the environment may interfere with glycemic metabolism by increasing hepatic glucose production in dams and their offspring.…”

Section: Liver Histology In Male F1 Offspringmentioning

confidence: 99%

See 1 more Smart Citation

Exposure to glyphosate-based herbicide during early stages of development increases insulin sensitivity and causes liver inflammation in adult mice offspring

Gomes¹,

Teleken²,

Vargas³

et al. 2022

Einstein (São Paulo)

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Objective: To investigate the effect of pre and postnatal exposure to a glyphosate-based herbicide on glucose metabolism and liver histology in adult F1 mice offspring. Methods: Female mice (C57Bl/6) received 0.5% of glyphosate (Roundup Original DI ® ) in drinking water or purified water (Glyphosate Group and Control Group respectively) during pregnancy and lactation. Offspring (F1) were submitted to glucose and insulin tolerance tests and euthanized on postnatal day 150. Body and plasma parameters, and liver histology were analyzed. Results: Exposure to glyphosate reduced maternal body weight gain during pregnancy and lactation, with no impacts on litter size. Pre and postnatal exposure to glyphosate did not affect body parameters but increased glucose tolerance on postnatal day 60. In spite of glucose tolerance normalization by postnatal day 143, this effect was associated with higher insulin sensitivity relative to mice in the Control-F1 Group. Mice in the Glyphosate-F1 Group had mild and moderate lobular inflammation in the liver. Conclusion: Maternal exposure to glyphosate affected insulin sensitivity and caused hepatic inflammation in adult F1 mice offspring.

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Section: Liver Histology In Male F1 Offspringmentioning

confidence: 48%

Section: Liver Histology In Male F1 Offspringmentioning

confidence: 99%

Exposure to glyphosate-based herbicide during early stages of development increases insulin sensitivity and causes liver inflammation in adult mice offspring

Gomes¹,

Teleken²,

Vargas³

et al. 2022

Einstein (São Paulo)

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“…It is important to note that hyperinsulinemia may eventually lead to insulin resistance and, therefore, may contribute to obesity and T2DM development ( 33 , 100 ). In contrast, other reports described decreased plasma insulin levels after exposing mice to 100 μg/kg/day BPA for 20 days ( 101 ) or 28 days ( 102 ), or even unchanged plasma insulin levels after 8 months of BPA administration (5–5,000 μg/kg/day) ( 103 ). These discrepancies in the observed outcomes might be due to the use of different mouse strains and/or variations in the administration protocol.…”

Section: Metabolic Consequences Of Adult Exposure To Bpamentioning

confidence: 88%

Timing of Exposure and Bisphenol-A: Implications for Diabetes Development

et al. 2018

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Bisphenol-A (BPA) is one of the most widespread endocrine disrupting chemicals (EDCs). It is used as the base compound in the production of polycarbonate and other plastics present in many consumer products. It is also used as a building block in epoxy can coating and the thermal paper of cash register receipts. Humans are consistently exposed to BPA and, in consequence, this compound has been detected in the majority of individuals examined. Over the last decade, an enlarging body of evidence has provided a strong support for the role of BPA in the etiology of diabetes and other metabolic disorders. Timing of exposure to EDCs results crucial since it has important implications on the resulting adverse effects. It is now well established that the developing organisms are particularly sensitive to environmental influences. Exposure to EDCs during early life may result in permanent adverse consequences, which increases the risk of developing chronic diseases like diabetes in adult life. In addition to that, developmental abnormalities can be transmitted from one generation to the next, thus affecting future generations. More recently, it has been proposed that gestational environment may also program long-term susceptibility to metabolic disorders in the mother. In the present review, we will comment and discuss the contributing role of BPA in the etiology of diabetes. We will address the metabolic consequences of BPA exposure at different stages of life and comment on the final phenotype observed in different whole-animal models of study.

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“…In resin-based composites and sealants in dentistry, BPA levels were reported to range from 0.5 to 84.4 μg per 100 mg of commercial product, and the saliva samples obtained after treatment using these products contained 3.3 to 30.0 μg/mL (approximately 14.5 to 131.4 μM) [ 32 ]. In some animal studies, long-term exposure to 0.1–10 mg/kg/day BPA decreased plasma insulin levels and increased the number of active caspase-3- positive cells in the pancreatic islets (approximately 0.44–43.8 μM/day), which accelerated DM development [ 33 , 34 ]. More importantly, MBP, as an active metabolite of BPA, is formed upon coincubation of BPA and liver microsomal and cytosolic fractions (S9 fraction from mammalian liver samples, including human samples) [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

4-Methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene, a Major Active Metabolite of Bisphenol A, Triggers Pancreatic β-Cell Death via a JNK/AMPKα Activation-Regulated Endoplasmic Reticulum Stress-Mediated Apoptotic Pathway

Huang

Yang

et al. 2021

IJMS

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4-methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene (MBP), a major active metabolite of bisphenol A (BPA), is generated in the mammalian liver. Some studies have suggested that MBP exerts greater toxicity than BPA. However, the mechanism underlying MBP-induced pancreatic β-cell cytotoxicity remains largely unclear. This study demonstrated the cytotoxicity of MBP in pancreatic β-cells and elucidated the cellular mechanism involved in MBP-induced β-cell death. Our results showed that MBP exposure significantly reduced cell viability, caused insulin secretion dysfunction, and induced apoptotic events including increased caspase-3 activity and the expression of active forms of caspase-3/-7/-9 and PARP protein. In addition, MBP triggered endoplasmic reticulum (ER) stress, as indicated by the upregulation of GRP 78, CHOP, and cleaved caspase-12 proteins. Pretreatment with 4-phenylbutyric acid (4-PBA; a pharmacological inhibitor of ER stress) markedly reversed MBP-induced ER stress and apoptosis-related signals. Furthermore, exposure to MBP significantly induced the protein phosphorylation of JNK and AMP-activated protein kinase (AMPK)α. Pretreatment of β-cells with pharmacological inhibitors for JNK (SP600125) and AMPK (compound C), respectively, effectively abrogated the MBP-induced apoptosis-related signals. Both JNK and AMPK inhibitors also suppressed the MBP-induced activation of JNK and AMPKα and of each other. In conclusion, these findings suggest that MBP exposure exerts cytotoxicity on β-cells via the interdependent activation of JNK and AMPKα, which regulates the downstream apoptotic signaling pathway.

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Co-exposure to endocrine disruptors: effect of bisphenol A and soy extract on glucose homeostasis and related metabolic disorders in male mice

Abstract: Soy extract may protect against some adverse effects of BPA. These findings represent the first report suggesting a potential effect between soy extract and BPA in low doses, however, further studies are needed to confirm these results.

Cited by 9 publications

References 46 publications

Exposure to glyphosate-based herbicide during early stages of development increases insulin sensitivity and causes liver inflammation in adult mice offspring

Exposure to glyphosate-based herbicide during early stages of development increases insulin sensitivity and causes liver inflammation in adult mice offspring

Timing of Exposure and Bisphenol-A: Implications for Diabetes Development

4-Methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene, a Major Active Metabolite of Bisphenol A, Triggers Pancreatic β-Cell Death via a JNK/AMPKα Activation-Regulated Endoplasmic Reticulum Stress-Mediated Apoptotic Pathway

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