Fig. 5.

PPARγ activation increases 3T3-L1 GIPR expression in differentiated adipocytes. 3T3-L1 preadipocytes were treated for 7 days with conditional culture medium 10 (see . Following differentiation, adipocytes were treated with the indicated concentrations of rosiglitazone (µM) for 20 h in the presence or absence of the inhibitor GW9662 (20 μM). A: Effects of PPARγ agonist and antagonist on nuclear PPARγ expression are shown. Nuclear extracts were isolated, and Western blot analyses were performed using antibodies against PPARγ and histone H3. B: Effects of PPARγ agonist and antagonist on adipocyte GIPR protein expression are shown. 3T3-L1 adipocytes were treated as described above, and Western blot analyses were performed using antibodies against GIPR and β-actin. C: Effects of PPARγ agonist and antagonist on adipocyte GIPR mRNA expression are shown. 3T3-L1 adipocytes were treated as described above, and real-time RT-PCR was performed to quantify GIPR mRNA levels, shown as the fold difference versus control normalized to 18S rRNA expression levels. All data represent three independent experiments, each carried out in duplicate, and Western blots are representative of n = 3 replicates. Significance was tested using ANOVA with Newman-Keuls post hoc test, where ** represents P <0.05 versus vehicle control with 0 μM rosiglitazone and 0 μM GW9662.