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Decrease in glucose transporter number in skeletal muscle of mildly diabetic (streptozotocin-treated) rats.
T Ramlal1, S Rastogi, M Vranic
1Department of Cell Biology, Hospital for Sick Children, Toronto, Ontario, Canada.
Endocrinology
|August 1, 1989
Summary
Diabetes reduces glucose transporters in muscle, impairing glucose uptake. Streptozotocin-induced diabetes in rats showed a significant decrease in plasma membrane glucose transporters, contributing to reduced glucose utilization.
Area of Science:
- Biochemistry
- Physiology
- Endocrinology
Background:
- Diabetes mellitus is characterized by impaired glucose metabolism.
- Skeletal muscle is a primary site for whole-body glucose uptake.
- Reduced muscle glucose uptake contributes to hyperglycemia in diabetes.
Purpose of the Study:
- To investigate the number of glucose transporters in skeletal muscle membranes of diabetic rats.
- To determine if a reduction in glucose transporters contributes to diminished glucose uptake in diabetes.
Main Methods:
- Streptozotocin (STZ) was used to induce diabetes in rats.
- Glucose transporter abundance was measured using [3H]cytochalasin-B binding assays in plasma and internal muscle membranes.
- Measurements were compared between control and diabetic rats.
Main Results:
- Diabetic rats exhibited a 37% decrease in total muscle membrane glucose transporters.
- Plasma membrane glucose transporters decreased by 50% in diabetic rats, while intracellular transporters decreased by 32%.
- Total plasma membrane transporters per gram of tissue decreased by 68% in diabetic rats.
Conclusions:
- Diabetes leads to a significant reduction in skeletal muscle glucose transporters, particularly in the plasma membrane.
- This depletion of glucose transporters likely contributes to the impaired glucose uptake observed in diabetic muscle.
- The findings suggest a molecular basis for reduced glucose utilization in diabetes.