PMID- 23998203
OWN - NLM
STAT- MEDLINE
DCOM- 20140728
LR  - 20131216
IS  - 1467-789X (Electronic)
IS  - 1467-7881 (Linking)
VI  - 15
IP  - 1
DP  - 2014 Jan
TI  - Persistent organic pollutants meet adipose tissue hypoxia: does cross-talk 
      contribute to inflammation during obesity?
PG  - 19-28
LID - 10.1111/obr.12086 [doi]
AB  - 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.
CI  - (c) 2013 The Authors. obesity reviews (c) 2013 International Association for the 
      Study of Obesity.
FAU - Myre, M
AU  - Myre M
AD  - Behavioral and Metabolic Research Unit, School of Human Kinetics, Faculty of 
      Health Sciences, University of Ottawa, Ottawa, Ontario, Canada.
FAU - Imbeault, P
AU  - Imbeault P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20130902
PL  - England
TA  - Obes Rev
JT  - Obesity reviews : an official journal of the International Association for the 
      Study of Obesity
JID - 100897395
RN  - 0 (Environmental Pollutants)
RN  - 0 (HIF1A protein, human)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
SB  - IM
MH  - Adipose Tissue/immunology/*metabolism/physiopathology
MH  - Adiposity
MH  - Animals
MH  - Cell Hypoxia/*immunology
MH  - Environmental Pollutants/adverse effects/immunology/*metabolism
MH  - Female
MH  - Humans
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/immunology/*metabolism
MH  - Inflammation/immunology
MH  - Inflammation Mediators/*metabolism
MH  - Male
MH  - Obesity/immunology/*metabolism/physiopathology
MH  - Polychlorinated Biphenyls/adverse effects/immunology/*metabolism
MH  - Rats
MH  - Receptor Cross-Talk/immunology
MH  - Receptors, Aryl Hydrocarbon/*metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - Aryl hydrocarbon receptor
OT  - hypoxia-inducible factor
OT  - oxygen deficit
OT  - xenobiotics
EDAT- 2013/09/04 06:00
MHDA- 2014/07/30 06:00
CRDT- 2013/09/04 06:00
PHST- 2013/06/05 00:00 [received]
PHST- 2013/07/08 00:00 [revised]
PHST- 2013/08/04 00:00 [accepted]
PHST- 2013/09/04 06:00 [entrez]
PHST- 2013/09/04 06:00 [pubmed]
PHST- 2014/07/30 06:00 [medline]
AID - 10.1111/obr.12086 [doi]
PST - ppublish
SO  - Obes Rev. 2014 Jan;15(1):19-28. doi: 10.1111/obr.12086. Epub 2013 Sep 2.