title: Persistent organic pollutants meet adipose tissue hypoxia: does cross-talk contribute to inflammation during obesity?
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.
authors.affiliation: Behavioral and Metabolic Research Unit, School of Human Kinetics, Faculty of Health Sciences, University of Ottawa, Ottawa, Ontario, Canada.
authors.forename: M
authors.initials: M
authors.lastname: Myre
authors.forename: P
authors.initials: P
authors.lastname: Imbeault
mesh_terms: D000273:Adipose Tissue / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D050154:Adiposity; D000818:Animals; D015687:Cell Hypoxia / Q000276:immunology*; D004785:Environmental Pollutants / Q000009:adverse effects / Q000276:immunology / Q000378:metabolism*; D005260:Female; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000276:immunology / Q000378:metabolism*; D007249:Inflammation / Q000276:immunology; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D009765:Obesity / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D011078:Polychlorinated Biphenyls / Q000009:adverse effects / Q000276:immunology / Q000378:metabolism*; D051381:Rats; D020239:Receptor Cross-Talk / Q000276:immunology; D018336:Receptors, Aryl Hydrocarbon / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D004785:Environmental Pollutants; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D018836:Inflammation Mediators; D018336:Receptors, Aryl Hydrocarbon; D011078:Polychlorinated Biphenyls
keywords: Aryl hydrocarbon receptor; hypoxia-inducible factor; oxygen deficit; xenobiotics