White adipose tissue: storage and effector site for environmental pollutants
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
16925464
DOI
10.33549/physiolres.931022
PII: 1022
Knihovny.cz E-resources
- MeSH
- Adipogenesis drug effects genetics MeSH
- Adipose Tissue, White drug effects metabolism physiopathology MeSH
- Endocrine Disruptors adverse effects MeSH
- Energy Metabolism drug effects genetics MeSH
- Transcription, Genetic drug effects MeSH
- Hormones metabolism MeSH
- Environmental Pollutants adverse effects classification metabolism MeSH
- Humans MeSH
- Polychlorinated Biphenyls adverse effects MeSH
- Polychlorinated Dibenzodioxins adverse effects analogs & derivatives MeSH
- Transcription Factors metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Endocrine Disruptors MeSH
- Hormones MeSH
- Environmental Pollutants MeSH
- Polychlorinated Biphenyls MeSH
- Polychlorinated Dibenzodioxins MeSH
- Transcription Factors MeSH
White adipose tissue (WAT) represents a reservoir of lipophilic environmental pollutants, especially of those which are resistant to biological and chemical degradation - so-called persistent organic pollutants (POPs). Large amounts of different congeners and isomers of these compounds exhibit a variety of adverse biological effects. Interactions among different classes of compounds, frequently with opposing effects, complicate hazard evaluation and risk assessment. WAT is the key organ for energy homeostasis and it also releases metabolites into the circulation and adipokines with systemic effects on insulin sensitivity and fuel partitioning in muscles and other tissues. Its beneficial role is lost in obesity when excessive accumulation of WAT contributes to severe diseases, such as diabetes. POPs may crossroad or modulate the effect of endogenous ligands of nuclear transcription factors, participating in differentiation, metabolism and the secretory function of adipocytes. These mechanisms include, most importantly: i) endocrine disrupting potency of POPs mixtures on androgen, estrogen or thyroid hormone metabolism/functions in WAT, ii) interference of dioxin-like chemicals with retinoic acid homeostasis, where impact on retinoid receptors is expected, and iii) interaction with transcriptional activity of peroxisome proliferator-activated receptors is likely. Thus, the accumulation and action of POPs in WAT represents a unitary mechanism explaining, at least in part, the effects of POPs in the whole organism. By modulating WAT differentiation, metabolism and function, the POPs could affect not only the physiological role of WAT, but they may also influence the development of obesity-associated diseases.
References provided by Crossref.org
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