Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants
Michele La Merrill,1 Claude Emond,2,3 Min Ji Kim,4,5,6,7 Jean-Philippe Antignac,8 Bruno Le Bizec,8 Karine Clément,9,10,11,12 Linda S. Birnbaum,13,14 and Robert Barouki4,5,6
1Department of Preventive Medicine, Mount Sinai School of Medicine, New York, New York, USA; 2BioSimulation Consulting Inc., Newark, Delaware, USA; 3Département de santé environnementale et santé au travail, Université de Montréal, Montréal, Québec, Canada; 4INSERM UMR-S 747, Paris, France; 5Université Paris Descartes, Centre Universitaire des Saints-Pères, Paris, France; 6Assistance Publique-Hôpitaux de Paris, Hôpital Necker-Enfants Malades, Paris, France; 7Université Paris 13, Sorbonne Paris Cité, INSERM U698, Bobigny, France; 8ONIRIS, USC 2013 INRA, LABERCA, Atlanpole-La Chantrerie, Nantes, France; 9INSERM, U872, Nutriomique équipe 7, Paris, France; 10Centre de Recherche des Cordeliers, Université Pierre et Marie Curie-Paris 6, UMR S 872, Paris, France; 11Assistance Publique-Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Département Nutrition et Endocrinologie, Paris, France; 12CRNH-Ile de France, Paris, France; 13National Cancer Institute, and 14National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA
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.
Key words: adipose tissue, aryl hydrocarbon receptor, development, diabetes, dioxin, inflammation, obesity, obesogens, polychlorinated biphenyls, toxicity, toxicokinetics.
Environ Health Perspect 121:162–169 (2013). http://dx.doi.org/10.1289/ehp.1205485 [Online 5 December 2012]
Address correspondence to R. Barouki, Université Paris Descartes, INSERM UMRS 747, Centre Universitaire des Saints-Pères, 45 rue des Saints Pères, 75270 Paris, Cedex 06, France. Telephone: 33 (0)1 42 86 20 75. E-mail: email@example.com
This study was funded by INSERM (Institut National de la Santé et de la Recherche Médicale), the National Institute of Environmental Health Sciences (NIEHS), the Université Paris Descartes, the Université Pierre et Marie Curie, and INRA (Institut National de la Recherche Agronomique).
The information in this document has been reviewed by the NIEHS and approved for publication. Approval does not signify that the contents necessarily reflect the views of the agency, nor does the mention of trade names or commercial products constitute endorsement or recommendation for use.
C.E. is employed by BioSimulation Consulting Inc., Newark, DE. The authors declare they have no actual or potential competing financial interests.
Received 17 May 2012; Accepted 4 December 2012; Online 5 December 2012.
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