Abstract
CELLULAR resistance to insulin caused by a reduction in insulinmediated glucose uptake can be produced in rats by chemically inducing diabetes with streptozotocin and by fasting1—3. Two glucose transporter isoforms are expressed in fat cells: (1) the insulin-responsive species4—8 which is found only in fat and muscle, and (2) a species corresponding to the erythrocyte/Hep G2/rat brain transporter9,10. We show here that fat cells isolated from streptozotocin diabetic rats and from fasted rats show a significant (60—80%) decrease in the amount of immunologically detectable insulin-sensitive glucose transporter and no change in the level of the Hep G2/rat brain transporter. Administration of insulin and refeeding, respectively, result in a return of the insulin-sensitive glucose transporter to levels that are normal or slightly above normal. Thus, peripheral tissue insulin resistance could be due to the specific reduction in the amount of insulin-sensitive glucose transporter.
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Berger, J., Biswas, C., Vicario, P. et al. Decreased expression of the insulin-responsive glucose transporter in diabetes and fasting. Nature 340, 70–72 (1989). https://doi.org/10.1038/340070a0
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DOI: https://doi.org/10.1038/340070a0
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