AGTR1 and Hyperglycemia: In β cells of pancreas, the deleterious axis of RAAS, i.e., Ang II-ACE-AT1R-aldosterone increases the oxidative stress, promotes apoptosis, decreases the uptake of glucose (by suppressing the GLUT2 through AT1R), and increases the production of ROS through NADPH oxidase (NOX), thereby decreasing the production of insulin leading to hyperglycemia (4).