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Toxicological function of adipose tissue: focus on persistent organic pollutants.

La Merrill M, Emond C, Kim MJ, Antignac JP, Le Bizec B, Clément K, Birnbaum LS, Barouki R - Environ. Health Perspect. (2012)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Preventive Medicine, Mount Sinai School of Medicine, New York, New York, USA.

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.

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Related in: MedlinePlus

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).
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f1: 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).

Mentions: Several human and animal studies have suggested that AT behaves as a toxicokinetic buffer for lipophilic pollutants (Figure 1). AT is a specific storage compartment for these pollutants. However, this is a dynamic situation, and release from AT occurs at a low basal level that can be magnified during weight loss. There is indirect evidence suggesting that released POPs exert some toxic effects (Kim et al. 2011); however, more direct evidence is needed.


Toxicological function of adipose tissue: focus on persistent organic pollutants.

La Merrill M, Emond C, Kim MJ, Antignac JP, Le Bizec B, Clément K, Birnbaum LS, Barouki R - Environ. Health Perspect. (2012)

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).
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3569688&req=5

f1: 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).
Mentions: Several human and animal studies have suggested that AT behaves as a toxicokinetic buffer for lipophilic pollutants (Figure 1). AT is a specific storage compartment for these pollutants. However, this is a dynamic situation, and release from AT occurs at a low basal level that can be magnified during weight loss. There is indirect evidence suggesting that released POPs exert some toxic effects (Kim et al. 2011); however, more direct evidence is needed.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Preventive Medicine, Mount Sinai School of Medicine, New York, New York, USA.

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.

Show MeSH
Related in: MedlinePlus