PMID- 16854242
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20070716
LR  - 20200928
IS  - 1743-7075 (Electronic)
IS  - 1743-7075 (Linking)
VI  - 3
DP  - 2006 Jul 19
TI  - Proinflammatory cytokine production and insulin sensitivity regulated by 
      overexpression of resistin in 3T3-L1 adipocytes.
PG  - 28
AB  - Resistin is secreted from adipocytes, and high circulating levels have been 
      associated with obesity and insulin resistance. To investigate whether resistin 
      could exert autocrine effects in adipocytes, we expressed resistin gene in 3T3-L1 
      fibroblasts using a lentiviral vector, and selected several stably-transduced 
      cell lines under blasticidin selection. We observed that 3T3-L1 adipocytes 
      expressing resistin have a decreased gene expression for related transcriptional 
      factors (CCAAT/enhancer binding protein alpha(C/EBPalpha), peroxisome 
      proliferator-activated receptor gamma (PPARgamma), and adipocyte lipid binding 
      protein (ALBP/aP2) which is one of target genes for the PPARgamma during 
      adipocyte differentiation,. Overexpression of resistin increased the levels of 
      three proinflammatory cytokines, tumor necrosis factor alpha (TNFalpha), 
      interleukin 6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1), which play 
      important roles for insulin resistance, glucose and lipid metabolisms during 
      adipogenesis. Furthermore, overexpressing resistin in adipocytes inhibits glucose 
      transport 4 (GLUT4) activity and its gene expression, reducing insulin's ability 
      for glucose uptake by 30%. In conclusion, resistin overexpression in stably 
      transduced 3T3-L1 cells resulted in: 1) Attenuation of programmed gene expression 
      responsible for adipogenesis; 2) Increase in expression of proinflammatory 
      cytokines; 3) Decrease in insulin responsiveness of the glucose transport system. 
      These data suggest a new role for resistin as an autocrine/paracrine factor 
      affecting inflammation and insulin sensitivity in adipose tissue.
FAU - Fu, Yuchang
AU  - Fu Y
AD  - Department of Nutrition Sciences, University of Alabama at Birmingham, 
      Birmingham, AL 35294-3360, USA. yfu@uab.edu
FAU - Luo, Liehong
AU  - Luo L
FAU - Luo, Nanlan
AU  - Luo N
FAU - Garvey, W Timothy
AU  - Garvey WT
LA  - eng
GR  - P01 HL055782/HL/NHLBI NIH HHS/United States
GR  - P30 DK056336/DK/NIDDK NIH HHS/United States
GR  - R01 DK038765/DK/NIDDK NIH HHS/United States
PT  - Journal Article
DEP - 20060719
PL  - England
TA  - Nutr Metab (Lond)
JT  - Nutrition & metabolism
JID - 101231644
PMC - PMC1550232
EDAT- 2006/07/21 09:00
MHDA- 2006/07/21 09:01
PMCR- 2006/07/19
CRDT- 2006/07/21 09:00
PHST- 2006/04/26 00:00 [received]
PHST- 2006/07/19 00:00 [accepted]
PHST- 2006/07/21 09:00 [pubmed]
PHST- 2006/07/21 09:01 [medline]
PHST- 2006/07/21 09:00 [entrez]
PHST- 2006/07/19 00:00 [pmc-release]
AID - 1743-7075-3-28 [pii]
AID - 10.1186/1743-7075-3-28 [doi]
PST - epublish
SO  - Nutr Metab (Lond). 2006 Jul 19;3:28. doi: 10.1186/1743-7075-3-28.