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Reduction of red cell glucose transporter intrinsic activity in diabetes running.
- Source :
-
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme [Horm Metab Res] 1994 Jan; Vol. 26 (1), pp. 26-32. - Publication Year :
- 1994
-
Abstract
- The function of the red blood cell glucose transporter was compared in samples from subjects with and without diabetes. Activity of the glucose transporting protein (GLUT-1) was measured by determining the first order rate constant for uptake of sorbose, a sugar transported by GLUT-1. Red cells were isolated from 13 patients with diabetes and 9 patients without diabetes and were washed free of intracellular glucose. The uptake rate constant was calculated from measurements of sorbose uptake at 0, 1, 2, 5 and 90 minutes at 37 degrees C. The rate constant was significantly decreased in cells isolated from patients with diabetes (0.242 vs 0.303 min-1 in non-diabetic subjects, p < 0.005). The number of GLUT-1 present per mg of membrane protein and clinical parameters such as weight, age, serum cholesterol and urea nitrogen were not significantly different between the groups. The rate constant per pmol of GLUT-1 was significantly decreased in the diabetic subjects. The relationship between diabetes control and the rate constant was not linear and there was no relationship between the calculated intrinsic activity and the HA1c. Because red cell GLUT-1 are not translocated and red cells do not synthesize new proteins, these data suggest that the intrinsic function of the glucose transporter from red cells of patients with diabetes is diminished. This may be due to alterations in the transporter or its membrane environment.
Details
- Language :
- English
- ISSN :
- 0018-5043
- Volume :
- 26
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme
- Publication Type :
- Academic Journal
- Accession number :
- 8150420
- Full Text :
- https://doi.org/10.1055/s-2007-1000767