Even though recruitment of glucose transporters (GLUT), such as GLUT3 and GLUT4, is increased in hyperthyroidism potentially leading to more glucose disposal in peripheral tissues, this might be overruled by insulin antagonistic actions of thyroid hormones, such as an increased glucose output from the liver and intestinal glucose absorption, decreased muscle glycogen storage, or upregulated glycogenolysis (2, 3, 25, 26, 27). The gene discussed is SLC2A1; the disease is hyperthyroidism.