Glucose transporters and diabetes

Abstract Peripheral insulin resistance is a characteristic feature of obesity and non-insulin-dependent diabetes mellitus (NIDDM), and the cause can be localized in part to a defect in glucose transport. GLUT4, the predominant glucose transporter in insulin sensitive tissues, undergoes striking tissue specific metabolic regulation; GLUT4 gene expression is reduced in adipocytes, and generally unchanged in muscle from insulin resistant humans and rodents. In adipocytes, lower levels of GLUT4 account for the glucose transport defect, whereas in muscle, impaired traffic or decreased function of GLUT4 at the plasma membrane may account for the defect. Future studies of GLUT4 translocation, fusion and exposure/activation will unravel the molecular mechanism(s) behind the development of insulin resistance.