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Relationship between erythrocyte GLUT1 function and membrane glycation in type 2 diabetes
M M Porter-Turner1, J C Skidmore, M A Khokher
1School of Health Sciences, University of Wolverhampton, Wolverhampton, UK.
British Journal of Biomedical Science
|January 24, 2012
Summary
Glycation impairs glucose transport in diabetic erythrocytes, reducing uptake and net transport despite unchanged transporter numbers. Binding affinity for glucose transporters increases in diabetes.
Area of Science:
- Physiology
- Biochemistry
- Endocrinology
Background:
- Glycation, a post-translational modification of proteins by sugars, is elevated in diabetes.
- Erythrocyte glucose transport is crucial for cellular glucose uptake and metabolic homeostasis.
- Understanding glycation's impact on glucose transporters is vital for managing diabetic complications.
Purpose of the Study:
- To investigate the effects of glycation on glucose transporter function, number, and phosphorylation in erythrocytes from diabetic patients.
- To compare glucose transport parameters between individuals with diabetes and healthy controls.
Main Methods:
- Simultaneous measurement of glucose transporter function, numbers, and erythrocyte phosphorylation rates.
- Utilized 3-O-methylglucose uptake, D-glucose influx, and 2-deoxyglucose phosphorylation assays.
- Quantified glucose transporter numbers and binding affinity using cytochalasin B studies.
Main Results:
- Significantly reduced 3-O-methylglucose uptake, D-glucose influx, and net transport in diabetic erythrocytes.
- No significant difference in erythrocyte phosphorylation rates or the number of functional glucose transporters.
- Increased binding affinity (lower K(d)) of glucose transporters in diabetic individuals.
- Negative correlation between HbA1c levels and D-glucose influx.
Conclusions:
- Glycation significantly impairs glucose transport function in erythrocytes, independent of transporter number.
- Increased glucose transporter binding affinity in diabetes may represent a compensatory mechanism.
- These findings highlight altered erythrocyte glucose metabolism in diabetes, potentially impacting glycemic control.
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