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.
Berger
J
J
Department of Biochemical Endocrinology, Merck Institute for Therapeutic Research, Rahway, New Jersey 07065.
Biswas
C
C
Vicario
P P
PP
Strout
H V
HV
Saperstein
R
R
Pilch
P F
PF
D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D005215:Fasting; D015151:Immunoblotting; D007333:Insulin Resistance; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D009004:Monosaccharide Transport Proteins