Prenatal Exposure to BPA and Offspring Outcomes
Obesity and type 2 diabetes mellitus (T2DM) are the most common metabolic disorders, with prevalence rates that are reaching epidemic proportions. Both are complex conditions affecting virtually all ages and with serious health consequences. The underlying cause of the problem is still puzzling, but...
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doaj-ce55a444e8ec4d2d81d96fe7732412f62020-11-25T02:33:59ZengSAGE PublishingDose-Response1559-32582015-06-011310.1177/155932581559039510.1177_1559325815590395Prenatal Exposure to BPA and Offspring OutcomesPaloma Alonso-Magdalena0Iván Quesada1Ángel Nadal2CIBER de Diabetes y Enfermedades Metabólicas Asociadas, CIBERDEM, Universidad Miguel Hernández de Elche, Elche, Alicante, SpainInstituto de Bioingeniería, Universidad Miguel Hernández de Elche, Elche, Alicante, SpainInstituto de Bioingeniería, Universidad Miguel Hernández de Elche, Elche, Alicante, SpainObesity and type 2 diabetes mellitus (T2DM) are the most common metabolic disorders, with prevalence rates that are reaching epidemic proportions. Both are complex conditions affecting virtually all ages and with serious health consequences. The underlying cause of the problem is still puzzling, but both genetic and environmental factors including unhealthy diet, sedentary lifestyle, or the exposure to some environmental endocrine disrupting chemicals (EDCs) are thought to have a causal influence. In addition, the impact of early environment has recently emerged as an important factor responsible for the increased propensity to develop adult-onset metabolic disease. Suboptimal maternal nutrition during critical windows in fetal development is the most commonly studied factor affecting early programming of obesity and T2DM. In recent years, increasing experimental evidence shows that exposure to EDCs could also account for this phenomenon. In the present review, we will overview the most relevant findings that confirm the critical role of bisphenol-A, one of the most widespread EDCs, in the development of metabolic disorders.https://doi.org/10.1177/1559325815590395 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Paloma Alonso-Magdalena Iván Quesada Ángel Nadal |
spellingShingle |
Paloma Alonso-Magdalena Iván Quesada Ángel Nadal Prenatal Exposure to BPA and Offspring Outcomes Dose-Response |
author_facet |
Paloma Alonso-Magdalena Iván Quesada Ángel Nadal |
author_sort |
Paloma Alonso-Magdalena |
title |
Prenatal Exposure to BPA and Offspring Outcomes |
title_short |
Prenatal Exposure to BPA and Offspring Outcomes |
title_full |
Prenatal Exposure to BPA and Offspring Outcomes |
title_fullStr |
Prenatal Exposure to BPA and Offspring Outcomes |
title_full_unstemmed |
Prenatal Exposure to BPA and Offspring Outcomes |
title_sort |
prenatal exposure to bpa and offspring outcomes |
publisher |
SAGE Publishing |
series |
Dose-Response |
issn |
1559-3258 |
publishDate |
2015-06-01 |
description |
Obesity and type 2 diabetes mellitus (T2DM) are the most common metabolic disorders, with prevalence rates that are reaching epidemic proportions. Both are complex conditions affecting virtually all ages and with serious health consequences. The underlying cause of the problem is still puzzling, but both genetic and environmental factors including unhealthy diet, sedentary lifestyle, or the exposure to some environmental endocrine disrupting chemicals (EDCs) are thought to have a causal influence. In addition, the impact of early environment has recently emerged as an important factor responsible for the increased propensity to develop adult-onset metabolic disease. Suboptimal maternal nutrition during critical windows in fetal development is the most commonly studied factor affecting early programming of obesity and T2DM. In recent years, increasing experimental evidence shows that exposure to EDCs could also account for this phenomenon. In the present review, we will overview the most relevant findings that confirm the critical role of bisphenol-A, one of the most widespread EDCs, in the development of metabolic disorders. |
url |
https://doi.org/10.1177/1559325815590395 |
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