Decreased expression of the insulin-responsive glucose transporter in diabetes and fasting

• DOI: 10.1038/340070a0
• Publication Date: 2003-06-12T22:20:24Z
• Authors: Joel Berger; Chhabi Biswas; Pasquale P. Vicario; H. Vincent Strout; Richard Saperstein; Paul F. Pilch
• Keywords: 0303 health sciences; 03 medical and health sciences; Adipose Tissue; Monosaccharide Transport Proteins; Immunoblotting; Animals; Rats, Inbred Strains; Fasting; Insulin Resistance; Diabetes Mellitus, Experimental; Rats

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.