Human and rodent muscle Na(+)-K(+)-ATPase in diabetes related to insulin, starvation, and training
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Human and rodent muscle Na(+)-K(+)-ATPase in diabetes related to insulin, starvation, and training. / Schmidt, T A; Hasselbalch, S; Farrell, P A; Vestergaard, H; Kjeldsen, K.
I: Journal of Applied Physiology, Bind 76, Nr. 5, 1994, s. 2140-6.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - Human and rodent muscle Na(+)-K(+)-ATPase in diabetes related to insulin, starvation, and training
AU - Schmidt, T A
AU - Hasselbalch, S
AU - Farrell, P A
AU - Vestergaard, H
AU - Kjeldsen, K
PY - 1994
Y1 - 1994
N2 - 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.
AB - 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.
KW - Adult
KW - Animals
KW - Cerebral Cortex
KW - Diabetes Mellitus
KW - Diabetes Mellitus, Experimental
KW - Diabetes Mellitus, Type 1
KW - Diabetes Mellitus, Type 2
KW - Female
KW - Humans
KW - Insulin
KW - Male
KW - Middle Aged
KW - Muscles
KW - Ouabain
KW - Pancreatectomy
KW - Physical Conditioning, Animal
KW - Rats
KW - Rats, Sprague-Dawley
KW - Rats, Wistar
KW - Sodium-Potassium-Exchanging ATPase
KW - Starvation
KW - Streptozocin
M3 - Journal article
C2 - 8063678
VL - 76
SP - 2140
EP - 2146
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
SN - 8750-7587
IS - 5
ER -
ID: 150332747