Decreased expression of the insulin-responsive glucose transporter in diabetes and fasting.
Cellular resistance to insulin caused by a reduction in insulin-mediated glucose uptake can be produced in rats by chemically inducing diabetes with streptozotocin and by fasting. Two glucose transporter isoforms are expressed in fat cells: (1) the insulin-responsive species which is found only in fat and muscle, and (2) a species corresponding to the erythrocyte/ Hep G2/rat brain transporter. 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.[1]References
- Decreased expression of the insulin-responsive glucose transporter in diabetes and fasting. Berger, J., Biswas, C., Vicario, P.P., Strout, H.V., Saperstein, R., Pilch, P.F. Nature (1989) [Pubmed]
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