DEMONSTRATION OF DEFECTIVE GLUCOSE-UPTAKE AND STORAGE IN ERYTHROCYTESFROM NON-INSULIN-DEPENDENT DIABETIC-PATIENTS AND EFFECTS OF METFORMIN

1. Red blood cells can store glucose and may thus participate in blood glucose homeostasis. We investigated if a defect in this process exis ts in non-insulin dependent diabetes (NIDD). 2. Blood was obtained in fasting conditions from 10 normal and 10 newly diagnosed NIDD patients (before and after 4 weeks Metformin therapy). Washed erythrocytes wer e resuspended in media containing various glucose concentrations (4.4, 6.6, 8.8 and 13.2 mmol/L). Total glucose uptake was calculated as the sum of the measurements of lactate as well as free glucose, the latte r being determined before and after addition of amyloglucosidase to th e pellet. 3. Cells from diabetics showed a pronounced reduction in glu cose uptake, particularly in their capacity to store glucose as glycog en (reactive to amyloglucosidase). Metformin treatment almost normaliz ed glycogen levels, whereas lactate declined concomitantly in the pell et. 4. Our data demonstrate that a defect in glucose uptake exists in erythrocytes from NIDD patients, affecting both free and stored glucos e, and that this defect is reversed by Metformin treatment, indicating that this drug can increase glycogen levels even in insulin-insensiti ve cells. 5. Thus, in view of their total mass, erythrocytes may be im portant in the impaired glucose homeostasis in NIDD, in particular in marked hyperglycaemia such as after a meal.