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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

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.
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f2: 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.

Mentions: POPs as obesogens. With the study of obesogens still in its infancy, experimental research on POPs as obesogens is sparse. In a recent review of the literature on developmental exposures that increase risk of obesity, with an emphasis on human exposures, we found that themes are already emerging (La Merrill and Birnbaum 2011). Development (e.g., prenatal, postnatal, pubertal) is likely a critical window of susceptibility to obesogen effects of toxic exposures (Figure 2). Programming mechanisms are still unclear but are believed to involve epigenetic regulation of critical genes that lead to adiposity later in life (Barouki et al. 2012). Evidence suggests that developmental exposures to chemicals that increase the risk of obesity sometimes operate in a nonmonotonic dose–response manner; cachexia may occur at high doses, whereas body and/or adipose mass gain occurs at low doses of the same chemical. Further, there may be sex-specific effects of developmental toxic exposures that increase the risk of obesity (Tang-Peronard et al. 2011). Here, we focus on experimental research on POPs that cause obesity and dyslipidemia. Developmental exposures to these same POPs are positively associated with obesity in humans (Valvi et al. 2012).


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)

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

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

f2: 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.
Mentions: POPs as obesogens. With the study of obesogens still in its infancy, experimental research on POPs as obesogens is sparse. In a recent review of the literature on developmental exposures that increase risk of obesity, with an emphasis on human exposures, we found that themes are already emerging (La Merrill and Birnbaum 2011). Development (e.g., prenatal, postnatal, pubertal) is likely a critical window of susceptibility to obesogen effects of toxic exposures (Figure 2). Programming mechanisms are still unclear but are believed to involve epigenetic regulation of critical genes that lead to adiposity later in life (Barouki et al. 2012). Evidence suggests that developmental exposures to chemicals that increase the risk of obesity sometimes operate in a nonmonotonic dose–response manner; cachexia may occur at high doses, whereas body and/or adipose mass gain occurs at low doses of the same chemical. Further, there may be sex-specific effects of developmental toxic exposures that increase the risk of obesity (Tang-Peronard et al. 2011). Here, we focus on experimental research on POPs that cause obesity and dyslipidemia. Developmental exposures to these same POPs are positively associated with obesity in humans (Valvi et al. 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.

Show MeSH
Related in: MedlinePlus