PMID- 17922949
OWN - NLM
STAT- MEDLINE
DCOM- 20080222
LR  - 20071009
IS  - 0007-1145 (Print)
IS  - 0007-1145 (Linking)
VI  - 98 Suppl 1
DP  - 2007 Oct
TI  - Altered signalling and gene expression associated with the immune system and the 
      inflammatory response in obesity.
PG  - S121-6
AB  - White adipose tissue functions not only as an energy store but also as an 
      important endocrine organ and is involved in the regulation of many pathological 
      processes. The obese state is characterised by a low-grade systemic inflammation, 
      mainly a result of increased adipocyte as well as fat resident- and 
      recruited-macrophage activity. In the past few years, various products of adipose 
      tissue including adipokines and cytokines have been characterised and a number of 
      pathways linking adipose tissue metabolism with the immune system have been 
      identified. In obesity, the pro- and anti-inflammatory effects of adipokines and 
      cytokines through intracellular signalling pathways mainly involve the nuclear 
      factor kappa B (NF-kappaB) and the Jun N-terminal kinase (JNK) systems as well as 
      the I kappa B kinase beta (IKK-beta). Mitogen-activated protein kinase (MAPK) and 
      extracellular-signal-regulated kinase (ERK) pathways, which lead to signal 
      transducer and activator of transcription 3 (STAT3) activation, are also 
      important in the production of pro-inflammatory cytokines. Obesity increases the 
      expression of leptin and other cytokines, as well as some macrophage and 
      inflammatory markers, and decreases adiponectin expression in adipose tissue. A 
      number of cytokines, e.g. tumour necrosis factor alpha (TNF-alpha) and monocyte 
      chemotactic protein 1 (MCP-1), and some pro-inflammatory interleukins, leuckocyte 
      antigens, chemochines, surface adhesion molecules and metalloproteases are 
      up-regulated whereas other factors are down-regulated. The present paper will 
      focus on the molecular mechanisms linking obesity and inflammation with emphasis 
      on the alteration of signalling and gene expression in adipose cell components.
FAU - Gil, Angel
AU  - Gil A
AD  - Institute of Nutrition and Food Technology, Department of Biochemistry and 
      Molecular Biology, University of Granada, Granada, Spain. agil@ugr.es
FAU - Maria Aguilera, Concepcion
AU  - Maria Aguilera C
FAU - Gil-Campos, Mercedes
AU  - Gil-Campos M
FAU - Canete, Ramon
AU  - Canete R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Br J Nutr
JT  - The British journal of nutrition
JID - 0372547
RN  - 0 (Inflammation Mediators)
SB  - IM
MH  - Gene Expression Regulation/*immunology
MH  - Humans
MH  - Inflammation/*etiology/genetics/immunology
MH  - Inflammation Mediators/metabolism
MH  - Obesity/complications/*immunology
MH  - Signal Transduction/immunology
RF  - 37
EDAT- 2007/11/21 09:00
MHDA- 2008/02/23 09:00
CRDT- 2007/11/21 09:00
PHST- 2007/11/21 09:00 [pubmed]
PHST- 2008/02/23 09:00 [medline]
PHST- 2007/11/21 09:00 [entrez]
AID - S0007114507838050 [pii]
AID - 10.1017/S0007114507838050 [doi]
PST - ppublish
SO  - Br J Nutr. 2007 Oct;98 Suppl 1:S121-6. doi: 10.1017/S0007114507838050.