Our previous results demonstrated that tungstate decreased weight gain and adiposity in obese rats through increased thermogenesis and lipid oxidation, suggesting that brown adipose tissue was one of the targets of its anti-obesity effect. To identify potential targets of tungstate, we used DIGE to compare brown adipose tissue protein extracts from the following experimental groups: untreated lean, tungstate treated lean, untreated obese and tungstate treated obese rats. In order to distinguish between direct targets of tungstate action from those that are secondary to body weight loss, we also included in the analysis an additional group consisting of obese rats that lose weight by caloric restriction. Hierarchical clustering of Anova and T-test contrasts clearly separated the different experimental groups. DIGE analysis identified 20 proteins as tungstate obesity-direct targets, involved in: Krebs cycle, glycolysis, lipolysis and fatty acid oxidation, electron transport and redox. Protein oxidation was decreased by tungstate treatment which confirmed a role in redox processes; however palmitate oxidation, as a measure of fatty acid beta oxidation, was not altered by tungstate, thus questioning its putative function on fatty acid oxidation. Protein network analyses using Ingenuity pathways highlighted peroxisome proliferator activated receptor  coactivator 1 alpha (PGC-1 alpha) as a potential target. We confirmed by real-time PCR that indeed tungstate up-regulates PGC-1 alpha and its major target, uncoupling protein 1, was also increased as shown by western blot. These results illustrate the utility of proteomics and bioinformatics approaches to identify targets of obesity therapies, and suggest that in brown adipose tissue, tungstate modulates redox processes and increases energy dissipation through uncoupling and PGC-1 alpha up-regulation, thus contributing to its overall anti-obesity effect.