Peripheral insulin resistance is a characteristic feature of obesity a
nd non-insulin-dependent diabetes mellitus (NIDDM), and the cause can
be localized in part to a defect in glucose transport. GLUT4, the pred
ominant glucose transporter in insulin sensitive tissues, undergoes st
riking tissue specific metabolic regulation; GLUT4 gene expression is
reduced in adipocytes, and generally unchanged in muscle from insulin
resistant humans and rodents. rn adipocytes, lower levels of GLUT4 acc
ount for the glucose transport defect, whereas in muscle, impaired tra
ffic or decreased function of GLUT4 at the plasma membrane may account
for the defect. Future studies of GLUT4 translocation, fusion and exp
osure/activation will unravel the molecular mechanism(s) behind the de
velopment of insulin resistance. (C) 1996 Academic Press Ltd