In this line, some authors have ascertained increased catabolism of glucose due to GLUT4 translocation to the plasma membrane in muscle and brown adipose cells [19,20], with up-regulation of the uncoupling protein-1 in brown adipose tissue and hepatic gluconeogenesis [25,26], causing as a result hyperinsulinemia or enhancement of peripheral glucose utilization [19,27,28]. The gene discussed is SLC2A4; the disease is hyperinsulinism.