Persistent organic pollutants meet adipose tissue hypoxia: does cross-talk contribute to inflammation during obesity?
Obes Rev
; 15(1): 19-28, 2014 Jan.
Article
en En
| MEDLINE
| ID: mdl-23998203
ABSTRACT
Lipophilic persistent organic pollutants (POPs) accumulate in lipid-rich tissues such as human adipose tissue. This is particularly problematic in individuals with excess adiposity, a physiological state that may be additionally characterized by local adipose tissue hypoxia. Hypoxic patches occur when oxygen diffusion is insufficient to reach all hypertrophic adipocytes. POPs and hypoxia independently contribute to the development of adipose tissue-specific and systemic inflammation often associated with obesity. Inflammation is induced by increased proinflammatory mediators such as tumour necrosis factor-alpha, interleukin-6, and monocyte chemotactic protein-1, as well as reduced adiponectin release, an anti-inflammatory and insulin-sensitizing adipokine. The aryl hydrocarbon receptor (AhR) mediates the cellular response to some pollutants, while hypoxia responses occur through the oxygen-sensitive transcription factor hypoxia-inducible factor (HIF)-1. There is some overlap between the two signalling pathways since both require a common subunit called the AhR nuclear translocator. As such, it is unclear how adipocytes respond to simultaneous POP and hypoxia exposure. This brief review explores the independent contribution of POPs and adipose tissue hypoxia as factors underlying the inflammatory response from adipocytes during obesity. It also highlights that the combined effect of POPs and hypoxia through the AhR and HIF-1 signalling pathways remains to be tested.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Asunto principal:
Hipoxia de la Célula
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Tejido Adiposo
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Bifenilos Policlorados
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Receptores de Hidrocarburo de Aril
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Mediadores de Inflamación
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Contaminantes Ambientales
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Subunidad alfa del Factor 1 Inducible por Hipoxia
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Obesidad
Límite:
Animals
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Female
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Humans
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Male
Idioma:
En
Revista:
Obes Rev
Asunto de la revista:
METABOLISMO
Año:
2014
Tipo del documento:
Article
País de afiliación:
Canadá