Genomics and Proteomics of Angiotensin II-Induced Insulin Resistance inOver-nutrition and Hypertension: Diabetes and metabolic syndrome drive the epidemic of cardiovascular diseases (CVD) causing a severe strain on our health care system. Angiotensin II (Ang II) is a vasoconstrictive, pro-growth and -inflammatory hormone that promotes both insulin resistance and CVD by activation of the Ang II type 1 receptor (AT1R). Clinical trials indicate therapies targeting Ang II biosynthesis and/or AT1R blockade (ARBs) are not as efficacious as expected, especially in patients with diabetes. A less investigated component of Ang II-signaling is the Ang II type 2 receptor (AT2R) that has anti-inflammatory properties and exerts antagonistic effects on AT1R signaling. Goal of this research is to unravel novel signaling pathways activated by the AT2R to regulate insulin resistance in conditions of over-nutrition and hypertension. We utilize rodent models for metabolic syndrome and ventricular myocyte-specific AT2R over-expression (AT2R TG mouse), primary culturing, transcription profiling (mRNA and miRNA), analysis of post-translational modifications, and ShRNA- and proteomic- approaches to determine how AT2R mediated signaling cross-talk with signaling activated by the nutrient sensors and other components of Renin-Angiotensin System.