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Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants

Background: Adipose tissue (AT) is involved in several physiological functions, including metabolic regulation, energy storage, and endocrine functions. Objectives: In this review we examined the evidence that an additional function of AT is to modulate persistent organic pollutant (POP) toxicity th...

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Autores principales: La Merrill, Michele, Emond, Claude, Kim, Min Ji, Antignac, Jean-Philippe, Le Bizec, Bruno, Clément, Karine, Birnbaum, Linda S., Barouki, Robert
Formato: Online Artículo Texto
Lenguaje:English
Publicado: National Institute of Environmental Health Sciences 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569688/
https://www.ncbi.nlm.nih.gov/pubmed/23221922
http://dx.doi.org/10.1289/ehp.1205485
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author La Merrill, Michele
Emond, Claude
Kim, Min Ji
Antignac, Jean-Philippe
Le Bizec, Bruno
Clément, Karine
Birnbaum, Linda S.
Barouki, Robert
author_facet La Merrill, Michele
Emond, Claude
Kim, Min Ji
Antignac, Jean-Philippe
Le Bizec, Bruno
Clément, Karine
Birnbaum, Linda S.
Barouki, Robert
author_sort La Merrill, Michele
collection PubMed
description Background: Adipose tissue (AT) is involved in several physiological functions, including metabolic regulation, energy storage, and endocrine functions. Objectives: In this review we examined the evidence that an additional function of AT is to modulate persistent organic pollutant (POP) toxicity through several mechanisms. Methods: We reviewed the literature on the interaction of AT with POPs to provide a comprehensive model for this additional function of AT. Discussion: As a storage compartment for lipophilic POPs, AT plays a critical role in the toxicokinetics of a variety of drugs and pollutants, in particular, POPs. By sequestering POPs, AT can protect other organs and tissues from POPs overload. However, this protective function could prove to be a threat in the long run. The accumulation of lipophilic POPs will increase total body burden. These accumulated POPs are slowly released into the bloodstream, and more so during weight loss. Thus, AT constitutes a continual source of internal exposure to POPs. In addition to its buffering function, AT is also a target of POPs and may mediate part of their metabolic effects. This is particularly relevant because many POPs induce obesogenic effects that may lead to quantitative and qualitative alterations of AT. Some POPs also induce a proinflammatory state in AT, which may lead to detrimental metabolic effects. Conclusion: AT appears to play diverse functions both as a modulator and as a target of POPs toxicity.
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spelling pubmed-35696882013-02-14 Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants La Merrill, Michele Emond, Claude Kim, Min Ji Antignac, Jean-Philippe Le Bizec, Bruno Clément, Karine Birnbaum, Linda S. Barouki, Robert Environ Health Perspect Review Background: Adipose tissue (AT) is involved in several physiological functions, including metabolic regulation, energy storage, and endocrine functions. Objectives: In this review we examined the evidence that an additional function of AT is to modulate persistent organic pollutant (POP) toxicity through several mechanisms. Methods: We reviewed the literature on the interaction of AT with POPs to provide a comprehensive model for this additional function of AT. Discussion: As a storage compartment for lipophilic POPs, AT plays a critical role in the toxicokinetics of a variety of drugs and pollutants, in particular, POPs. By sequestering POPs, AT can protect other organs and tissues from POPs overload. However, this protective function could prove to be a threat in the long run. The accumulation of lipophilic POPs will increase total body burden. These accumulated POPs are slowly released into the bloodstream, and more so during weight loss. Thus, AT constitutes a continual source of internal exposure to POPs. In addition to its buffering function, AT is also a target of POPs and may mediate part of their metabolic effects. This is particularly relevant because many POPs induce obesogenic effects that may lead to quantitative and qualitative alterations of AT. Some POPs also induce a proinflammatory state in AT, which may lead to detrimental metabolic effects. Conclusion: AT appears to play diverse functions both as a modulator and as a target of POPs toxicity. National Institute of Environmental Health Sciences 2012-12-05 2013-02 /pmc/articles/PMC3569688/ /pubmed/23221922 http://dx.doi.org/10.1289/ehp.1205485 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 Review
La Merrill, Michele
Emond, Claude
Kim, Min Ji
Antignac, Jean-Philippe
Le Bizec, Bruno
Clément, Karine
Birnbaum, Linda S.
Barouki, Robert
Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants
title Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants
title_full Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants
title_fullStr Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants
title_full_unstemmed Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants
title_short Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants
title_sort toxicological function of adipose tissue: focus on persistent organic pollutants
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569688/
https://www.ncbi.nlm.nih.gov/pubmed/23221922
http://dx.doi.org/10.1289/ehp.1205485
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