Resistin is known as an adipocyte-specific secretory hormone that can cause 
insulin resistance and decrease adipocyte differentiation. It can be regulated 
by sexual hormones. Whether environmental estrogens regulate the production of 
resistin is still not clear. Using 3T3-L1 adipocytes, we found that octylphenol 
upregulated resistin mRNA expression in dose- and time-dependent manners. The 
concentration of octylphenol that increased resistin mRNA levels by 50% was 
approximately 100 nM within 6 h of treatment. The basal half-life of resistin 
mRNA induced by actinomycin D was lengthened by octylphenol treatment, 
suggesting that octylphenol decreases the rate of resistin mRNA degradation. In 
addition, octylphenol stimulated resistin protein expression and release. The 
basal half-life of resistin protein induced by cycloheximide was lengthened by 
octylphenol treatment, suggesting that octylphenol decreases the rate of 
resistin protein degradation. While octylphenol was shown to increase activities 
of the estrogen receptor (ER) and MEK1, signaling was demonstrated to be blocked 
by pretreatment with either ICI-182780 (an ERalpha antagonist) or U-0126 (a MEK1 
inhibitor), in which both inhibitors prevented octylphenol-stimulated 
phosphorylation of ERK. These results imply that ERalpha and ERK are necessary 
for the octylphenol stimulation of resistin mRNA expression. Moreover, U-0126 
antagonized the octylphenol-increased resistin protein expression and release. 
These data suggest that the way octylphenol signaling increases resistin protein 
levels is similar to that by which it increases resistin mRNA levels; it is 
likely mediated through an ERK-dependent pathway. In vivo, octylphenol increased 
adipose resistin mRNA expression and serum resistin and glucose levels, 
supporting its in vitro effect.