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Thyroid hormone action on glucose transporter activity in astrocytes
L M Roeder1, I B Hopkins, J R Kaiser
1Department of Pediatrics, University of Maryland, School of Medicine, Baltimore.
Biochemical and Biophysical Research Communications
|October 14, 1988
Summary
Thyroid hormone (L-T3) deficiency reduces glucose transporter binding in rat brain astrocytes. Supplementation with L-T3 increases transporter accessibility, suggesting hormone activation of glucose transport.
Area of Science:
- Neuroscience
- Cell Biology
- Endocrinology
Background:
- Astrocytes play crucial roles in brain energy metabolism.
- Glucose transporters are vital for nutrient uptake in brain cells.
- Thyroid hormones influence cellular function and metabolism.
Purpose of the Study:
- To investigate the effect of thyroid hormone deficiency on glucose transporter binding in rat brain astrocytes.
- To determine if L-T3 influences the accessibility of glucose transporter binding sites.
Main Methods:
- Culturing rat brain astrocytes in thyroid hormone-deficient media.
- Measuring cytochalasin B binding to assess glucose transporter levels.
- Using saponin treatment to evaluate the accessibility of binding sites.
- Analyzing binding in intact cells and plasma membrane fractions.
Main Results:
- Cytochalasin B binding decreased by 80% in thyroid hormone-deficient astrocytes.
- L-T3 supplementation restored binding to 75% of control levels.
- Saponin treatment increased binding site accessibility, suggesting L-T3 deficiency reduces total glucose transporters.
- L-T3 addition converted 90% of binding sites from unavailable to accessible.
Conclusions:
- Thyroid hormone deficiency significantly impairs glucose transporter function in astrocytes.
- L-T3 appears to activate glucose transporters primarily by increasing their accessibility.
- These findings highlight a novel regulatory role for thyroid hormone in brain glucose metabolism.