In the liver, IR is manifested by the blunted ability of insulin to suppress hepatic glucose production.2 Mice with hepatocytes lacking insulin receptors showed severe glucose intolerance and impaired ability of insulin to inhibit liver glucose output.3 During fasting, glycolysis is inhibited but fatty acid oxidation (FAO) and gluconeogenesis in the liver are increased, which is critical to maintain the glucostasis. This evidence concerns the gene INS and Glucose intolerance.