HUMAN AND RODENT MUSCLE NA-K+-ATPASE IN DIABETES-RELATED TO INSULIN, STARVATION, AND TRAINING()

As determined by vanadate-facilitated [H-3]ouabain binding to intact s amples, semistarvation and untreated streptozotocin- or partial pancre atectomy-induced diabetes reduced rat soleus muscle Na+-K+-adenosinetr iphosphatase (Na+-(K)+-ATPase) concentration by 12-21% (P < 0.05). Con versely, insulin treatment of rats with streptozotocin-induced diabete s induced an increase of 18-26% above control (P < 0.05). Treadmill tr aining diminished the reduction in muscle [H-3]ouabain binding site co ncentration induced by untreated diabetes to only 2-5%. No significant variation was observed in rat cerebral cortex Na+-K+-ATPase concentra tion as a result of diabetes, semistarvation, or insulin treatment. In human subjects, Na+-K+-ATPase concentration in vastus lateralis muscl e biopsies was 17 and 22% greater (P < 0.05), respectively, in patient s with treated non-insulin-dependent diabetes mellitus (n = 24) and in sulin-dependent diabetes mellitus (n = 7) than in control subjects (n = 8). A positive linear correlation between muscle Na+-K+-ATPase and p lasma insulin concentrations was observed (r = 0.50, P = 0.006; n = 29 ). Thus, insulin seems a regulator of muscle Na+-K+-ATPase concentrati on, reduction of muscle Na+-K+-ATPase concentration with untreated dia betes bears similarities with undernourishment, and physical condition ing may ameliorate the muscle Na+-K+-ATPase concentration decrease ind uced by diabetes.