Glucose is fundamental to the metabolism of mammalian cells. Its passage
across cell membranes is mediated by a family of transporters termed glucose
transporters or Gluts. In adipose and muscle tissue, insulin stimulates
a rapid and dramatic increase in glucose uptake, which is largely due to
the redistribution of the insulin-inducible glucose transporter, Glut4. In
response to insulin, Glut4 is quickly shuttled from an intracellular storage
site to the plasma membrane, where it binds glucose. In contrast, the ubiquitously
expressed glucose transporter Glut1 is constitutively targeted to the
plasma membrane and shows a much less dramatic translocation in response
to insulin. Glut1 and Glut4 are twelve pass transmembrane proteins
(12TM) whose carboxy-termini may dictate their cellular localization. Aberrant
Glut4 expression has been suggested to contribute to such maladies as obesity
and diabetes. Glut4 null mice have shown that while functional Glut4 protein
is not required for maintaining normal glucose levels, it is necessary for
sustained growth, normal cellular glucose, fat metabolism and prolonged
longevity.