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Bisphenol-A and metabolic diseases: epigenetic developmental and transgenerational basis
Departamento de Biología Aplicada, Universidad Miguel Hernández.
Laboratory of Stem Cells and Neurogeneration, Institute of Anatomy, Histology and Pathology, Facultu of Medicine and Center for INterdiciplinary Studies on the Nervous System (CISNe), Universitad Austral de Chile; Institute for Molecular Regenerative MEdicine and Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus University, Salzburg, Austira.
Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
2016 (English)In: Environmental Epigenetics, ISSN 2058-5888, Vol. 2, no 3, 1-10 p.Article in journal (Refereed) Published
Abstract [en]

Exposure to environmental toxicants is now accepted as a factor contributing to the increasing incidence of obesity and metabolic diseases around the world. Such environmental compounds are known as ‘obesogens’. Among them, bisphenol-A (BPA) is the most widespread and ubiquitous compound affecting humans and animals. Laboratory animal work has provided conclusive evidence that early-life exposure to BPA is particularly effective in predisposing individuals to weight gain. Embryonic exposure to BPA is reported to generate metabolic disturbances later in life, such as obesity and diabetes. When BPA administration is combined with a high-fat diet, there is an exacerbation in the development of metabolic disorders. Remarkably, upon BPA exposure of gestating females, metabolic disturbances have been found both in the offspring and later in life in the mothers themselves. When considering the metabolic effects generated by an early developmental exposure to BPA, one of the questions that arises is the role of precursor cells in the etiology of metabolic disorders. Current evidence shows that BPA and other endocrine disruptors have the ability to alter fat tissue development and growth by affecting the capacity to generate functional adipocytes, as well as their rate of differentiation to specific cell types. Epigenetic mechanisms seem to be involved in the BPA-induced effects related to obesity, as they have been described in both in vitro and in vivo models. Moreover, recent reports also show that developmental exposure to BPA generates abnormalities that can be transmitted to future generations, in a process called as transgenerational epigenetic inheritance.

Place, publisher, year, edition, pages
Oxford University Press, 2016. Vol. 2, no 3, 1-10 p.
Keyword [en]
BPA, Obesity, metabolic diseases, epigenetics, mesenchymal stem cells, transgenerational
National Category
Biological Sciences
URN: urn:nbn:se:liu:diva-132275OAI: diva2:1040016
Available from: 2016-10-26 Created: 2016-10-26 Last updated: 2016-11-15Bibliographically approved

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Guerrero Bosagna, Carlos
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