title: Human and rodent muscle Na(+)-K(+)-ATPase in diabetes related to insulin, starvation, and training.
abstract: As determined by vanadate-facilitated [3H]ouabain binding to intact samples, semistarvation and untreated streptozotocin- or partial pancreatectomy-induced diabetes reduced rat soleus muscle Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) concentration by 12-21% (P < 0.05). Conversely, insulin treatment of rats with streptozotocin-induced diabetes induced an increase of 18-26% above control (P < 0.05). Treadmill training diminished the reduction in muscle [3H]ouabain binding site concentration induced by untreated diabetes to only 2-5%. No significant variation was observed in rat cerebral cortex Na(+)-K(+)-ATPase concentration as a result of diabetes, semistarvation, or insulin treatment. In human subjects, Na(+)-K(+)-ATPase concentration in vastus lateralis muscle biopsies was 17 and 22% greater (P < 0.05), respectively, in patients with treated non-insulin-dependent diabetes mellitus (n = 24) and insulin-dependent diabetes mellitus (n = 7) than in control subjects (n = 8). A positive linear correlation between muscle Na(+)-K(+)-ATPase and plasma insulin concentrations was observed (r = 0.50, P = 0.006; n = 29). Thus, insulin seems a regulator of muscle Na(+)-K(+)-ATPase concentration, reduction of muscle Na(+)-K(+)-ATPase concentration with untreated diabetes bears similarities with undernourishment, and physical conditioning may ameliorate the muscle Na(+)-K(+)-ATPase concentration decrease induced by diabetes.
authors.affiliation: Laboratory for Human Performance Research, Pennsylvania State University, University Park 16802.
authors.forename: T A
authors.initials: TA
authors.lastname: Schmidt
authors.forename: S
authors.initials: S
authors.lastname: Hasselbalch
authors.forename: P A
authors.initials: PA
authors.lastname: Farrell
authors.forename: H
authors.initials: H
authors.lastname: Vestergaard
authors.forename: K
authors.initials: K
authors.lastname: Kjeldsen
mesh_terms: D000328:Adult; D000818:Animals; D002540:Cerebral Cortex / Q000201:enzymology; D003920:Diabetes Mellitus / Q000201:enzymology*; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology*; D003922:Diabetes Mellitus, Type 1 / Q000201:enzymology; D003924:Diabetes Mellitus, Type 2 / Q000201:enzymology; D005260:Female; D006801:Humans; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000201:enzymology*; D010042:Ouabain / Q000493:pharmacokinetics; D010180:Pancreatectomy; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013217:Starvation / Q000201:enzymology*; D013311:Streptozocin
chemical_list: D007328:Insulin; D010042:Ouabain; D013311:Streptozocin; D000254:Sodium-Potassium-Exchanging ATPase