SLC2A4 and hyperinsulinism: In response to insulin (and exercise in skeletal muscle), GLUT4 rapidly translocates from an intracellular pool to the cell surface to facilitate glucose uptake.36 Genetic ablation of GLUT4 in mice results in severe postprandial insulin resistance, hyperinsulinemia, and hyperglycaemia.37 Our results demonstrate that genetic variation directly influencing SLC2A4 expression has a significant impact on human postprandial insulin action.