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Timing of Exposure and Bisphenol-A: Implications for Diabetes Development
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 regis...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6220716/ https://www.ncbi.nlm.nih.gov/pubmed/30429829 http://dx.doi.org/10.3389/fendo.2018.00648 |
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author | Tudurí, Eva Marroqui, Laura Dos Santos, Reinaldo S. Quesada, Iván Fuentes, Esther Alonso-Magdalena, Paloma |
author_facet | Tudurí, Eva Marroqui, Laura Dos Santos, Reinaldo S. Quesada, Iván Fuentes, Esther Alonso-Magdalena, Paloma |
author_sort | Tudurí, Eva |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6220716 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-62207162018-11-14 Timing of Exposure and Bisphenol-A: Implications for Diabetes Development Tudurí, Eva Marroqui, Laura Dos Santos, Reinaldo S. Quesada, Iván Fuentes, Esther Alonso-Magdalena, Paloma Front Endocrinol (Lausanne) Endocrinology 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. Frontiers Media S.A. 2018-10-31 /pmc/articles/PMC6220716/ /pubmed/30429829 http://dx.doi.org/10.3389/fendo.2018.00648 Text en Copyright © 2018 Tudurí, Marroqui, Dos Santos, Quesada, Fuentes and Alonso-Magdalena. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Endocrinology Tudurí, Eva Marroqui, Laura Dos Santos, Reinaldo S. Quesada, Iván Fuentes, Esther Alonso-Magdalena, Paloma Timing of Exposure and Bisphenol-A: Implications for Diabetes Development |
title | Timing of Exposure and Bisphenol-A: Implications for Diabetes Development |
title_full | Timing of Exposure and Bisphenol-A: Implications for Diabetes Development |
title_fullStr | Timing of Exposure and Bisphenol-A: Implications for Diabetes Development |
title_full_unstemmed | Timing of Exposure and Bisphenol-A: Implications for Diabetes Development |
title_short | Timing of Exposure and Bisphenol-A: Implications for Diabetes Development |
title_sort | timing of exposure and bisphenol-a: implications for diabetes development |
topic | Endocrinology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6220716/ https://www.ncbi.nlm.nih.gov/pubmed/30429829 http://dx.doi.org/10.3389/fendo.2018.00648 |
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