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The percentage of the control value was calculated using measured rates (in nanomoles per gram per minute) for all experimental treatments. Data were analysed using a two-way ANOVA with insulin treatment (basal versus insulin) and genotype (control siRNA versus RIP140 siRNA) as factors. The Tukey�CKramer test for post hoc multiple comparisons was performed where appropriate. In all instances, an �� value of 0.05 [http://www.selleckchem.com/products/epz-6438.html EPZ6438] was used to determine significance. Downregulation of RIP140 by siRNA treatment was confirmed using RT-PCR and Western blotting analysis as a marker of end-point protein expression. Total RIP140 mRNA and protein content were affected by both treatment with insulin (P [http://en.wikipedia.org/wiki/Montelukast Montelukast Sodium] we measured basal and insulin-mediated glucose uptake and FA uptake and oxidation in cells treated with the siRNA Silencer Negative sequence (control siRNAgroup) with those of cells not treated with siRNA (untransfected control group). Neither basal nor insulin-mediated glucose and palmitate uptake and oxidation were different (P > 0.05) between groups (data not shown). In line with published data (Dyck et al. 2001; Luiken et al. 2002; Kelly et al. 2008), insulin significantly (P [http://www.selleckchem.com/Akt.html selleck screening library] and oxidation were measured in L6 cells with downregulated expression of RIP140 (RIP140 siRNA) and compared with the responses of cells treated with the siRNA negative control (control siRNA) sequence (Fig. 2). Glucose uptake was affected by insulin (P= 0.01) but not by genotype (P= 0.34). In both control siRNA- and RIP140 siRNA-treated cells, insulin increased glucose uptake (by 30�C31%). Interaction effects between insulin and genotype were uncovered for palmitate uptake (P= 0.02) and oxidation (P= 0.0006). In the basal state, RIP140 downregulation significantly increased (P