Hyperpolarization of muscle by insulin in a glucose-free environment

1959 ◽  
Vol 197 (3) ◽  
pp. 524-526 ◽  
Author(s):  
Kenneth L. Zierler

In a glucose-free solution, insulin increased resting membrane potential of rat extensor digitorum longus muscle by as much as it had in the presence of glucose. Even in the absence of glucose there was probably net accumulation of potassium by muscle, but the increase in muscle potassium concentration was too small to have been the cause of the observed hyperpolarization. It is concluded that insulin hyperpolarizes muscle membrane, as a result of which potassium moves into muscle, and that the eventual effect of insulin on potassium movement can be independent of any effect insulin may also have on glucose uptake.

1960 ◽  
Vol 198 (5) ◽  
pp. 1066-1070 ◽  
Author(s):  
Kenneth L. Zierler

Potassium efflux from rat extensor digitorum longus muscle was measured by counting the decrease in K42 in muscle bathed in K42-free solution. The rate constant for K efflux was 0.27 hr.–1 at 37°C and 0.16 hr.–1 at 26°C. Insulin decreased the rate constant for K efflux to 0.22 hr.–1 at 37°C and to 0.09 hr.–1 at 26°C. The effect of insulin on efflux was quantitatively the same when glucose was removed from the bathing solution. From measurement of net change in intracellular K and from measurement of changes in the driving potential for K it is concluded that insulin probably also decreases K influx, but to a lesser degree. However, when half the chloride is removed from the bathing solution, efflux and influx are decreased equally. The data can be interpreted by the hypothesis that insulin increases the positive fixed charge within the muscle membrane.


1959 ◽  
Vol 197 (3) ◽  
pp. 515-523 ◽  
Author(s):  
Kenneth L. Zierler

Insulin increased resting membrane potential of excised rat muscle, extensor digitorum longus, by about 5 mv in less than 1 hour. In 1 hour insulin caused no increase in the ratio of intra- to extracellular potassium, but in 2–3 hours intracellular K increased by about 10%. It is concluded that the increase in intracellular K is probably too small and too late to account for the hyperpolarization on the basis of conventional theory and it is suggested that the hyperpolarization produced by insulin is the cause of the potassium shift.


2009 ◽  
pp. 599-603 ◽  
Author(s):  
O Tyapkina ◽  
E Volkov ◽  
L Nurullin ◽  
B Shenkman ◽  
I Kozlovskaya ◽  
...  

Antiorthostatic hindlimb suspension (unloading) decreased the resting membrane potential (RMP) of skeletal muscle fibers in fast extensor digitorum longus (EDL) and slow soleus (SOL) muscle of the rat by about 10 % within 7 days and more. Inactivation of the membrane Na+, K+-pump by ouabain brought about similar depolarization as unloading. The increased sodium permeability of the membrane was excluded as the major cause of this depolarization by experiments in which TRIS was substituted for Na+ in the medium. On the other hand, the decrease in the electrogenic participation of the Na+,K+-pump is apparently one of the causes of RMP decrease during hypogravity, in EDL muscle in particular.


1979 ◽  
Vol 236 (5) ◽  
pp. E519 ◽  
Author(s):  
M N Goodman ◽  
N B Ruderman

The effects of starvation and of aging on the sensitivity of skeletal muscle to insulin were studied in the isolated perfused rat hindquarter preparation. As we have shown previously, starvation for 48 h had no effect on glucose uptake in hindquarters perfused with high levels of insulin (5 and 20 mU/ml). On the other hand, in the presence of physiological concentrations of insulin (50--200 muU/ml), glucose utilization was substantially greater in starved rats. Low concentrations of insulin had a greater effect on glucose uptake in fed young (100-g) than in fed older (350-g) rats. Starvation for 48 h enhanced glucose uptake in both young and older rats; however, the relative differences persisted. Starvation had similar effects on glucose utilization by the incubated soleus and extensor digitorum longus muscle. In addition, it augmented the stimulation by insulin of alpha-aminoisobutyric acid transport into the incubated extensor digitorum longus muscle. These results suggest that the in vitro sensitivity of skeletal muscle to physiological concentrations of insulin is enhanced during starvation. The basis for these findings and their physiological implications remain to be determined.


1971 ◽  
Vol 121 (5) ◽  
pp. 817-827 ◽  
Author(s):  
R. C. Hider ◽  
E. B. Fern ◽  
D. R. London

1. The kinetics of radioactive labelling of extra- and intra-cellular amino acid pools and protein of the extensor digitorum longus muscle were studied after incubations with radioactive amino acids in vitro. 2. The results indicated that an extracellular pool could be defined, the contents of which were different from those of the incubation medium. 3. It was concluded that amino acids from the extracellular pool, as defined in this study, were incorporated directly into protein.


1995 ◽  
Vol 269 (5) ◽  
pp. R1154-R1162 ◽  
Author(s):  
A. D. Kriketos ◽  
D. A. Pan ◽  
J. R. Sutton ◽  
J. F. Hoh ◽  
L. A. Baur ◽  
...  

Insulin resistance in skeletal muscle is associated with 1) relative increases in the proportion of glycolytic and fast-twitch muscle fibers and decreases in the proportion of more oxidative fibers and 2) a higher proportion of the saturated fatty acids in membrane structural lipids. Exercise is known to improve insulin action. The aims of the current studies were 1) to investigate the relationship between muscle fiber type and membrane fatty acid composition and 2) to determine how voluntary exercise might influence both variables. In sedentary Wistar rats in experiment 1, increased amounts of unsaturated fatty acids were found in the more oxidative insulin-sensitive red quadriceps and soleus muscles, whereas reduced levels of polyunsaturated fatty acids were found in primarily glycolytic white quadriceps muscles. In experiment 2, voluntary running-wheel exercise by adult female rats over 45 days resulted in reduced proportions of type IIb fibers (P = 0.01) and increased proportions of type IIa/IIx fibers (P = 0.03) in extensor digitorum longus muscle. The magnitude of these changes was related to the distance run (r = -0.73, P = 0.04; r = 0.79, P = 0.02, respectively). Exercise significantly increased oxidative capacity, as assessed by the proportion of intensely NADH-stained fibers (P = 0.0004) and citrate synthase (P = 0.003) and hexokinase (P = 0.04) activities. Citrate synthase activity was also increased by exercise in soleus muscle, where, as expected, no fiber type changes were detected. No significant differences in the fatty acid profile of soleus and extensor digitorum longus were found between groups.(ABSTRACT TRUNCATED AT 250 WORDS)


2000 ◽  
Vol 203 (14) ◽  
pp. 2229-2236 ◽  
Author(s):  
M.W. Beaumont ◽  
E.W. Taylor ◽  
P.J. Butler

Previously, the distribution of ammonia between the intracellular and extracellular compartments has been used to predict a significant depolarisation of the resting membrane potential (E(M)) of white muscle from brown trout (Salmo trutta) exposed to a sub-lethal combination of copper and low pH. However, this prediction is based upon two assumptions (i) a relatively high membrane permeability for the ammonium ion with respect to that for ammonia gas and (ii) that this is unaltered by exposure to copper and low pH. Since there is conflicting evidence in the literature of the validity of these assumptions, in the present study E(M) was directly measured in white muscle fibres of trout exposed to copper and low pH (E(M)=−52.2+/−4.9 mV) and compared with that of unexposed, control animals (E(M)=−86.5+/−2.9 mV) (means +/− s.e.m., N=6). In confirming the predicted depolarisation, these data support the hypothesis of electrophysiological impairment as a factor in the reduction in the swimming performance of trout exposed to these pollutants. In addition, the results of this study support the role of a significant permeability of the muscle membrane to NH(4)(+) in determining the distribution of ammonia in fish.


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