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J. Biol. Chem., Vol. 265, Issue 12, 6548-6551, 04, 1990
JH Johnson, CB Newgard, JL Milburn, HF Lodish and B Thorens
The liver has been shown to contain a facilitated diffusion glucose
transporter with high Km for glucose that is structurally distinct from the
low Km glucose transporters found in most other tissues. We find that
3-O-methyl glucose is greater than 90% equilibrated across dispersed islet
cells within 60 s, consistent with a facilitated diffusion transport
mechanism. L-Glucose uptake was minimal throughout the time course,
indicating stereospecificity. Measurement of glucose transport over a range
of 3-O-methyl glucose concentrations from 0.05 to 60 mM revealed the
presence of a component of glucose transport with an apparent Km of 17 mM,
a value essentially identical to that previously reported for liver.
Interestingly, a second component of glucose transport was also observed
with an apparent Km of 1.4 mM, as has been reported for other tissues such
as erythrocytes that are known to contain the "HepG2" or "erythroid/brain"
type glucose transporter. Further evidence for the existence of two
transport components is provided by the observation that a low
concentration of cytochalasin B (0.4 microM) completely inhibits the low Km
transport activity but has no effect on the high Km transporter. The
kinetic similarity of high Km glucose transport in liver and islets is
readily understood in light of our structural analysis. Sequence analysis
of cDNA clones indicates that the liver and islet glucose transporters have
identical sequences and, thus, are the products of the same gene.
The high Km glucose transporter of islets of Langerhans is functionally similar to the low affinity transporter of liver and has an identical primary sequence
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.
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