White adipose tissue: storage and effector site for environmental pollutants
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
PubMed
16925464
DOI
10.33549/physiolres.931022
PII: 1022
Knihovny.cz E-zdroje
- MeSH
- adipogeneze účinky léků genetika MeSH
- bílá tuková tkáň účinky léků metabolismus patofyziologie MeSH
- endokrinní disruptory škodlivé účinky MeSH
- energetický metabolismus účinky léků genetika MeSH
- genetická transkripce účinky léků MeSH
- hormony metabolismus MeSH
- látky znečišťující životní prostředí škodlivé účinky klasifikace metabolismus MeSH
- lidé MeSH
- polychlorované bifenyly škodlivé účinky MeSH
- polychlorované dibenzodioxiny škodlivé účinky analogy a deriváty MeSH
- transkripční faktory metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- endokrinní disruptory MeSH
- hormony MeSH
- látky znečišťující životní prostředí MeSH
- polychlorované bifenyly MeSH
- polychlorované dibenzodioxiny MeSH
- transkripční faktory 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.
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