Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 Feb;121(2):162-9.
doi: 10.1289/ehp.1205485. Epub 2012 Dec 5.

Toxicological function of adipose tissue: focus on persistent organic pollutants

Michele La Merrill  1 , Claude Emond, Min Ji Kim, Jean-Philippe Antignac, Bruno Le Bizec, Karine Clément, Linda S Birnbaum, Robert Barouki
Affiliations
Review

Toxicological function of adipose tissue: focus on persistent organic pollutants

Michele La Merrill et al. Environ Health Perspect. 2013 Feb.

Abstract

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.

PubMed Disclaimer

Conflict of interest statement

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.

Figures

Figure 1
Figure 1
Dual role of AT in the regulation of POP kinetics. Upon exposure to POPs, these lipophilic pollutants are stored in liver and AT (left); this prevents the action of these pollutants in other sensitive tissues and may be protective to a certain extent. POPs released from their storage site in AT constitute a source of low-level internal exposure (right).
Figure 2
Figure 2
POPs as obesogens and as disruptors of AT structure and function. Strong evidence from both in vivo and in vitro studies suggests that POPs can influence the development of AT, particularly at low doses. These programming events take place in early life (e.g., fetal, neonatal), probably through epigenetic mechanisms, and could have an impact on diseases in adulthood. In addition, POPs can alter AT function and structure later in life; this occurs primarily through metabolic disruption and inflammation. These effects favor the development of metabolic diseases.
Figure 3
Figure 3
Major signaling mechanisms involved in the effects of DL POPs on AT. Abbreviations: ER, estrogen receptor; RAR, retinoic acid receptor. Most, if not all, of the effects of DL compounds are mediated by the AhR. Only genomic effects are shown. The AhR could directly regulate target genes as a heterodimer with ARNT. Several interactions with transcription factors or nuclear receptors that have been described are shown here. POPs could either trigger these interactions or disrupt existing interactions between the AhR and other signaling factors.
See this image and copyright information in PMC

Comment in

References

    1. Aarnio V, Storvik M, Lehtonen M, Asikainen S, Reisner K, Callaway J, et al. Fatty acid composition and gene expression profiles are altered in aryl hydrocarbon receptor-1 mutant Caenorhabditis elegans. Comp Biochem Physiol C Toxicol Pharmacol. 2010;151:318–324. - PubMed
    1. Antignac JP, Marchand P, Gade C, Matayron G, Qannari EM, Le Bizec B, et al. Studying variations in the PCDD/PCDF profile across various food products using multivariate statistical analysis. Anal Bioanal Chem. 2006;384:271–279. - PubMed
    1. Arsenescu V, Arsenescu RI, King V, Swanson H, Cassis LA. Polychlorinated biphenyl-77 induces adipocyte differentiation and proinflammatory adipokines and promotes obesity and atherosclerosis. Environ Health Perspect. 2008;116:761–768. - PMC - PubMed
    1. Baccarelli A, Wright RO, Bollati V, Tarantini L, Litonjua AA, Suh HH, et al. Rapid DNA methylation changes after exposure to traffic particles. Am J Respir Crit Care Med. 2009;179:572–578. - PMC - PubMed
    1. Barouki R. Linking long-term toxicity of xeno-chemicals with short-term biological adaptation. Biochimie. 2010;92:1222–1226. - PubMed

Publication types

MeSH terms

LinkOut - more resources