Insulin as Regulator of Skeletal Muscle Na+/K+-ATPase Concentration in Rats With Experimental Diabetes and Patients With Diabetes Mellitus

Using vanadate facilitated 3H-ouabain binding to intact samples it has earlier been demonstrated that untreated streptozotocin (STZ) induced diabetes in rats leads to a significant reduction in skeletal muscle Na+/K+-ATPase concentration (8). Aspects regarding Na+/K+-ATPase regulation in humans with diabetes have primarily been investigated using erythrocyte membranes. Both in IDDM (13,16) and NIDDM (10,11) a Na+/K+-ATPase decrease of around 30 % has previously been reported in erythrocytes. The attention should, however, be brought to the evidence that studies on erythrocyte membranes regarding Na+/K+-ATPase regulation need not mirror regulatory aspects of Na+/K+-ATPase in other tissues, and should generally not be expected to furnish data of general physiological impact (7,12,14). In e.g. K-depletion Na+/K+-ATPase concentration is reportedly upregulated in erythrocytes but downregulated in muscles. While skeletal muscle in adult human subjects contain 75% of the total body K, erythrocytes contain only 7%. Since furthermore skeletal muscle K continuously equilibrates substantially with blood, erythrocytes, thus, play only a minor role in plasma K regulation compared to skeletal muscle.