BACKGROUND INFORMATION: STAT3 (signal transducer and activator of transcription 
3) is an important transcription factor involved in many biological events, 
including apoptosis, tumorigenesis, angiogenesis and epithelial-to-mesenchymal 
transition. However, no direct evidence for a role of STAT3 in 3T3-L1 adipocyte 
differentiation has been reported.
RESULTS: In the present study, we found that rapid activation of STAT3, lasting 
for more than 48 h, was elicited upon induction of adipogenesis. Both the 
STAT3-selective inhibitor stattic and the JAK2 (Janus kinase 2)/STAT3-selective 
inhibitors AG490 and Gö6976 inhibited STAT3 activation, leading to the 
suppression of adipocyte differentiation. Adipocyte differentiation was also 
suppressed by STAT3 siRNA (small interfering RNA) or dominant-negative STAT3. 
Interestingly, the PPARgamma (peroxisome-proliferator-activated receptor gamma) 
agonist TAZ (troglitazone) abolished the STAT3-inhibitor- and RNAi (RNA 
interference)-mediated suppression of adipogenesis. However, TAZ treatment had 
no effect on the stattic- and AG490-mediated down-regulation of STAT3 
activation, suggesting that STAT3 regulates adipocyte differentiation through 
signalling that occurs upstream of PPARgamma.
CONCLUSION: These data indicate that STAT3 functions as a critical factor for 
adipogenesis via a mechanism involving the PPARgamma activation pathway.