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Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion
Bisphenol A (BPA) is an ubiquitous synthetic chemical exerting numerous adverse effects. Results of rodent studies show that BPA negatively affects adipose tissue. However, the short-term influence of this compound addressing adipocyte metabolism and adipokine secretion is unknown. In the present st...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8113171/ https://www.ncbi.nlm.nih.gov/pubmed/33447972 http://dx.doi.org/10.1007/s11356-021-12411-0 |
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author | Szkudelska, Katarzyna Okulicz, Monika Szkudelski, Tomasz |
author_facet | Szkudelska, Katarzyna Okulicz, Monika Szkudelski, Tomasz |
author_sort | Szkudelska, Katarzyna |
collection | PubMed |
description | Bisphenol A (BPA) is an ubiquitous synthetic chemical exerting numerous adverse effects. Results of rodent studies show that BPA negatively affects adipose tissue. However, the short-term influence of this compound addressing adipocyte metabolism and adipokine secretion is unknown. In the present study, isolated rat adipocytes were exposed for 2 h to 1 and 10 nM BPA. Insulin-induced glucose conversion to lipids along with glucose transport was significantly increased in the presence of BPA. However, basal glucose conversion to lipids, glucose oxidation, and formation of lipids from acetate were unchanged in adipocytes incubated with BPA. It was also shown that BPA significantly increases lipolytic response of adipocytes to epinephrine. However, lipolysis stimulated by dibutyryl-cAMP (a direct activator of protein kinase A) and the antilipolytic action of insulin were not affected by BPA. Moreover, BPA did not influence leptin and adiponectin secretion from adipocytes. Our new results show that BPA is capable of disturbing processes related to lipid accumulation in isolated rat adipocytes. This is associated with the potentiation of insulin and epinephrine action. The effects of BPA appear already after short-term exposure to low doses of this compound. However, BPA fails to change adipokine secretion. |
format | Online Article Text |
id | pubmed-8113171 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-81131712021-05-13 Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion Szkudelska, Katarzyna Okulicz, Monika Szkudelski, Tomasz Environ Sci Pollut Res Int Research Article Bisphenol A (BPA) is an ubiquitous synthetic chemical exerting numerous adverse effects. Results of rodent studies show that BPA negatively affects adipose tissue. However, the short-term influence of this compound addressing adipocyte metabolism and adipokine secretion is unknown. In the present study, isolated rat adipocytes were exposed for 2 h to 1 and 10 nM BPA. Insulin-induced glucose conversion to lipids along with glucose transport was significantly increased in the presence of BPA. However, basal glucose conversion to lipids, glucose oxidation, and formation of lipids from acetate were unchanged in adipocytes incubated with BPA. It was also shown that BPA significantly increases lipolytic response of adipocytes to epinephrine. However, lipolysis stimulated by dibutyryl-cAMP (a direct activator of protein kinase A) and the antilipolytic action of insulin were not affected by BPA. Moreover, BPA did not influence leptin and adiponectin secretion from adipocytes. Our new results show that BPA is capable of disturbing processes related to lipid accumulation in isolated rat adipocytes. This is associated with the potentiation of insulin and epinephrine action. The effects of BPA appear already after short-term exposure to low doses of this compound. However, BPA fails to change adipokine secretion. Springer Berlin Heidelberg 2021-01-14 2021 /pmc/articles/PMC8113171/ /pubmed/33447972 http://dx.doi.org/10.1007/s11356-021-12411-0 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Article Szkudelska, Katarzyna Okulicz, Monika Szkudelski, Tomasz Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion |
title | Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion |
title_full | Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion |
title_fullStr | Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion |
title_full_unstemmed | Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion |
title_short | Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion |
title_sort | bisphenol a disturbs metabolism of primary rat adipocytes without affecting adipokine secretion |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8113171/ https://www.ncbi.nlm.nih.gov/pubmed/33447972 http://dx.doi.org/10.1007/s11356-021-12411-0 |
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