Even though insulin resistance has emerged as an enormous health care problem, encompassing the fields of obesity, diabetes, hypertension, and cardiovascular diseases (1,2), its molecular mechanism remains incompletely understood. Clinically, the term insulin resistance implies that higher than normal concentrations of insulin are required to maintain normoglycemia. In other words, insulin-resistant humans and animals develop compensatory hyperinsulinemia in order to ensure normal utilization of glucose by the insulin target tissues (3). Physiologically, insulin is released from the pancreatic β-cells post-prandially in order to maintain euglycemia. Insulin promotes glucose uptake in skeletal muscle and fat by stimulating translocation of glucose transporter 4 (GLUT 4) from the cytosol to the plasma membrane where it facilitates glucose transport (4,5). Concomitantly, insulin stimulates intracellular utilization of glucose by many other tissues as well. Post-absorptively (i.e. in the fasting state), the main physiological task of insulin is to suppress glucose production by the liver. Therefore, if either of these main aspects of insulin action is impaired, one can encounter insulin resistance either at the level of skeletal muscle and fat or hepatic insulin resistance, both of which contribute to the total body insulin resistance.