Chronic dapagliflozin treatment lowered plasma glucose and insulin concentrations and reduced both tumor glucose uptake and VPDH/VCS in an insulin-dependent manner, whereas obesity increased tumor glucose metabolism and SGLT2 inhibition normalized it, the obesity- and hyperinsulinemia-associated increases in glucose uptake and oxidation were restored by chronic subcutaneous insulin infusion (Fig. 5b–e). The gene discussed is SLC5A2; the disease is hyperinsulinism.