Reduction of erythrocyte (Na+-K+)ATPase activity in Type 1 (insulin-dependent) diabetic subjects and its activation by homologous plasma

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Abstract
The (Na+-K+)ATPase and (Mg2+)ATPase activities of erythrocyte membranes of Type 1 (insulin-dependent) diabetic patients were found to be significantly reduced compared to matched controls (p < 0.005). On the contrary, erythrocyte Na+ and K+ contents were similar in diabetic patients and in normal subjects. When erythrocyte membranes from diabetic patients were incubated with their own plasma, a significant increase was observed in sodium-potassium ATPase activity (p < 0.005), whereas (Mg2+)ATPase activity was not affected. The plasma stimulatory effect showed saturation kinetics. Maximum average stimulation was 96% (±21.3). A similar stimulation pattern, although more limited in extent (maximum 48.3 % ± 12.2), was found when erythrocyte membranes from normal subjects were incubated with diabetic plasma. Normal plasma exhibited a modest stimulatory effect on erythrocyte (Na+-K+ATPase activity. Similar stimulatory effects by diabetic plasma were observed on a (Na+-K+) ATPase preparation from beef heart. It is proposed that diabetic plasma contains a specific (Na+-K+)ATPase activator in a higher concentration than normal plasma. This may explain why a normal cellular electrolyte content was found in diabetic erythrocytes in spite of a reduced Na+-K+ pump activity. Purification experiments indicate that the plasma activator is a protein with a molecular weight greater than 50,000. Both the (Na+-K+)ATPase activity and the stimulatory effect of diabetic plasma were not influenced by the metabolic control, since they did not correlate significantly with fasting blood glucose and daily insulin dosage. Moreover, no correlation was found with duration of diabetes or age at diagnosis of diabetes. It is suggested that the enzyme defect of erythrocyte membrane and the stimulation of (Na+-K+)ATPase activity by homologous plasma are early biochemical alterations in the course of diabetes mellitus.