Different [3H]ouabain binding characteristics of fast and slow skeletal muscles in IDDM and NIDDM diabetic rats.
The aim of this study was to determine the ouabain receptor density, sodium content and contractile properties of skeletal muscles in rats with insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus induced by streptozotocin treatment. These parameters were compared in isolated soleus (SOL) and extensor digitorum longus (EDL) muscles of diabetic animals and their age-matched controls. Reversibility of the diabetes-induced changes was studied by insulin or thyroxine substitution. In IDDM SOL muscles both the maximum [3H]ouabain binding capacity (Bmax) and dissociation constant (Kd) were decreased, the sodium content of the muscles increased and the velocity of contraction and relaxation decreased. Similar changes (except for the reduction of Bmax) were observed in diabetic EDL muscles; however, in this case these differences were less prominent. All of these changes were reversed by insulin substitution, whereas thyroxine treatment normalized only the changes in Bmax and velocity of contraction. In contrast to the changes observed in IDDM, NIDDM increased both Kd and Bmax values. Linear correlation was observed between the velocity of contraction or relaxation and the density of [3H]ouabain binding sites in the SOL muscles of IDDM rats. It is concluded that IDDM and NIDDM induce opposite alterations in the density and ouabain sensitivity of the Na(+)-K+ pump in rat skeletal muscle. These diabetic changes are fully reversible with insulin substitution, they are variable in size according to the type of muscle, and are also reflected in the sodium content and, ultimately, in the contractile parameters of the muscles.
Bányász
T
T
Department of Physiology, University Medical School of Debrecen, Hungary.
Kovács
T
T
D000375:Aging / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000378:metabolism* / Q000493:pharmacokinetics; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D009119:Muscle Contraction / Q000502:physiology; D018656:Muscle Fibers, Fast-Twitch / Q000201:enzymology / Q000378:metabolism*; D018657:Muscle Fibers, Slow-Twitch / Q000201:enzymology / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000166:cytology / Q000201:enzymology / Q000378:metabolism*; D010042:Ouabain / Q000378:metabolism* / Q000493:pharmacokinetics; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism; D013974:Thyroxine / Q000494:pharmacology
D001786:Blood Glucose; D004791:Enzyme Inhibitors; D007004:Hypoglycemic Agents; D007328:Insulin; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D013974:Thyroxine