The multiple hormonal imbalances observed in the Crh−120/+ mice can be attributed to both the direct and indirect effects of excess GCs in adipose tissue, skeletal muscle, liver, and pancreatic β-cells, which lead to increased plasma concentrations of leptin (Figure 5), reflecting increased fat mass; hyperinsulinemia indicating insulin resistance; and dysregulation of the counterregulatory hormone glucagon, which exacerbates the hyperglycemia. The gene discussed is LEP; the disease is hyperinsulinism.