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Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat

BACKGROUND: The causes of the current obesity pandemic have not been fully elucidated. Implication of environmental endocrine disruptors such as bisphenol A (BPA) on adipose tissue development has been poorly investigated. OBJECTIVES: The aim of the present study was to evaluate the effects of perin...

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Autores principales: Somm, Emmanuel, Schwitzgebel, Valérie M., Toulotte, Audrey, Cederroth, Christopher R., Combescure, Christophe, Nef, Serge, Aubert, Michel L., Hüppi, Petra S.
Formato: Texto
Lenguaje:English
Publicado: National Institute of Environmental Health Sciences 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790509/
https://www.ncbi.nlm.nih.gov/pubmed/20019905
http://dx.doi.org/10.1289/ehp.11342
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author Somm, Emmanuel
Schwitzgebel, Valérie M.
Toulotte, Audrey
Cederroth, Christopher R.
Combescure, Christophe
Nef, Serge
Aubert, Michel L.
Hüppi, Petra S.
author_facet Somm, Emmanuel
Schwitzgebel, Valérie M.
Toulotte, Audrey
Cederroth, Christopher R.
Combescure, Christophe
Nef, Serge
Aubert, Michel L.
Hüppi, Petra S.
author_sort Somm, Emmanuel
collection PubMed
description BACKGROUND: The causes of the current obesity pandemic have not been fully elucidated. Implication of environmental endocrine disruptors such as bisphenol A (BPA) on adipose tissue development has been poorly investigated. OBJECTIVES: The aim of the present study was to evaluate the effects of perinatal exposure to BPA on early adipose storage at weaning. METHODS: Pregnant Sprague-Dawley rats had access to drinking water containing 1 mg/L BPA from day 6 of gestation through the end of lactation. Pups were weaned on postnatal day (PND) 21. At that time, we investigated perigonadal adipose tissue of pups (weight, histology, gene expression). For the remaining animals, we recorded body weight and food intake for animals on either standard chow or a high-fat diet. RESULTS: Gestational exposure to BPA did not alter the sex ratio or litter size at birth. On PND1, the weight of male and female BPA-exposed pups was increased. On PND21, body weight was increased only in females, in which parametrial white adipose tissue (pWAT) weight was increased about 3-fold. This excess of pWAT was associated with adipocyte hypertrophy and overexpression of lipogenic genes such as C/EBP-α (CAAT enhancer binding protein alpha), PPAR-γ (peroxisome proliferator-activated receptor gamma), SREBP-1C (sterol regulatory element binding protein-1C), LPL (lipoprotein lipase), FAS (fatty acid synthase), and SCD-1 (stearoyl-CoA desaturase 1). In addition, gene expression of SREBP-1C, FAS, and ACC (acetyl-CoA carboxylase) was also increased in liver from BPA-exposed females at PND21, without a change in circulating lipids and glucose. After weaning, perinatal BPA exposure predisposed to overweight in a sex- and diet-dependent manner. We observed no change in food intake due to perinatal BPA exposure in rats on either standard chow or a high-fat diet. CONCLUSIONS: Perinatal exposure to a low dose of BPA increased adipogenesis in females at weaning. Adult body weight may be programmed during early life, leading to changes dependent on the sex and the nutritional status. Although further studies are required to understand the mechanisms of BPA action in early life, these results are particularly important with regard to the increasing prevalence of childhood obesity and the context-dependent action of endocrine disruptors.
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spelling pubmed-27905092009-12-17 Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat Somm, Emmanuel Schwitzgebel, Valérie M. Toulotte, Audrey Cederroth, Christopher R. Combescure, Christophe Nef, Serge Aubert, Michel L. Hüppi, Petra S. Environ Health Perspect Research BACKGROUND: The causes of the current obesity pandemic have not been fully elucidated. Implication of environmental endocrine disruptors such as bisphenol A (BPA) on adipose tissue development has been poorly investigated. OBJECTIVES: The aim of the present study was to evaluate the effects of perinatal exposure to BPA on early adipose storage at weaning. METHODS: Pregnant Sprague-Dawley rats had access to drinking water containing 1 mg/L BPA from day 6 of gestation through the end of lactation. Pups were weaned on postnatal day (PND) 21. At that time, we investigated perigonadal adipose tissue of pups (weight, histology, gene expression). For the remaining animals, we recorded body weight and food intake for animals on either standard chow or a high-fat diet. RESULTS: Gestational exposure to BPA did not alter the sex ratio or litter size at birth. On PND1, the weight of male and female BPA-exposed pups was increased. On PND21, body weight was increased only in females, in which parametrial white adipose tissue (pWAT) weight was increased about 3-fold. This excess of pWAT was associated with adipocyte hypertrophy and overexpression of lipogenic genes such as C/EBP-α (CAAT enhancer binding protein alpha), PPAR-γ (peroxisome proliferator-activated receptor gamma), SREBP-1C (sterol regulatory element binding protein-1C), LPL (lipoprotein lipase), FAS (fatty acid synthase), and SCD-1 (stearoyl-CoA desaturase 1). In addition, gene expression of SREBP-1C, FAS, and ACC (acetyl-CoA carboxylase) was also increased in liver from BPA-exposed females at PND21, without a change in circulating lipids and glucose. After weaning, perinatal BPA exposure predisposed to overweight in a sex- and diet-dependent manner. We observed no change in food intake due to perinatal BPA exposure in rats on either standard chow or a high-fat diet. CONCLUSIONS: Perinatal exposure to a low dose of BPA increased adipogenesis in females at weaning. Adult body weight may be programmed during early life, leading to changes dependent on the sex and the nutritional status. Although further studies are required to understand the mechanisms of BPA action in early life, these results are particularly important with regard to the increasing prevalence of childhood obesity and the context-dependent action of endocrine disruptors. National Institute of Environmental Health Sciences 2009-10 2009-06-29 /pmc/articles/PMC2790509/ /pubmed/20019905 http://dx.doi.org/10.1289/ehp.11342 Text en http://creativecommons.org/publicdomain/mark/1.0/ Publication of EHP lies in the public domain and is therefore without copyright. All text from EHP may be reprinted freely. Use of materials published in EHP should be acknowledged (for example, ?Reproduced with permission from Environmental Health Perspectives?); pertinent reference information should be provided for the article from which the material was reproduced. Articles from EHP, especially the News section, may contain photographs or illustrations copyrighted by other commercial organizations or individuals that may not be used without obtaining prior approval from the holder of the copyright.
spellingShingle Research
Somm, Emmanuel
Schwitzgebel, Valérie M.
Toulotte, Audrey
Cederroth, Christopher R.
Combescure, Christophe
Nef, Serge
Aubert, Michel L.
Hüppi, Petra S.
Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat
title Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat
title_full Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat
title_fullStr Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat
title_full_unstemmed Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat
title_short Perinatal Exposure to Bisphenol A Alters Early Adipogenesis in the Rat
title_sort perinatal exposure to bisphenol a alters early adipogenesis in the rat
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790509/
https://www.ncbi.nlm.nih.gov/pubmed/20019905
http://dx.doi.org/10.1289/ehp.11342
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