Effect of streptozotocin‐induced diabetes upon intracellular sodium in rat skeletal muscle

Moore, Richard D.; Munford, John; Popolizio, M.

doi:10.1016/0014-5793(79)80535-9

Cited by 17 publications

(5 citation statements)

References 18 publications

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“…The increased cellular sodium activity observed in diabetic patients might be caused by the impaired activity of the sodium pump, being consistent with the increase in intracellular sodium previously reported in rat skeletal muscle during streptozotocin-induced diabetes [38]. The lack of a close correlation between erythrocytic Na+ activity and Na+,K+-ATPase activity might be the consequence of a change of the membrane passive permeability to sodium or of the existence of multiple sodium transport mechanisms in the cell membrane, namely the Na+-Li+ countertransport and the Na+-K+ cotransport [12].…”

Section: Discussionsupporting

confidence: 91%

Modifications induced by diabetes on the physicochemical and functional properties of erythrocyte plasma membrane

Mazzanti

Rabini

Testa

et al. 1989

Eur J Clin Investigation

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Increasing evidence suggests that in experimental diabetes an impairment in Na+,K+-ATPase activity plays a central role in the pathophysiology of diabetic complications, while only a few data are available with regard to human subjects. We studied the erythrocyte membrane Na+,K+-ATPase activity and membrane fluidity in insulin-dependent and non-insulin-dependent diabetic subjects. A significant decrease in the enzyme activity and in fluorescence polarization values was found in both groups compared with normal subjects. Neither Na+,K+-ATPase activity nor membrane fluidity was found to be related to metabolic control, assessed by means of fasting blood glucose levels and HbA1c. On the contrary, a significant correlation was observed between Na+,K+-ATPase activity and membrane fluidity in both insulin-dependent and non-insulin-dependent diabetic subjects. The present work provides evidence that a reduction in the Na+,K+-ATPase activity is present in the plasma membranes of insulin-dependent and non-insulin-dependent diabetics. Furthermore, it suggests that the change in enzyme activity might be related to modifications in membrane fluidity.

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Section: Discussionsupporting

confidence: 91%

Modifications induced by diabetes on the physicochemical and functional properties of erythrocyte plasma membrane

Mazzanti

Rabini

Testa

et al. 1989

Eur J Clin Investigation

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“…of insulin must regulate the Na pump in vivo and thus hypoinsulinaemia, due to any cause, should result in decreased activity of the Na pump and thus produce an elevation of intracellular Na+. In a preliminary study Moore, Munford & Popolizio (1979) reported that levels of intracellular Na+ were, as predicted, increased in soleus muscles from streptozotocin, SZ, diabetic rats compared to muscles from sham-injected controls.…”

Section: Introductionmentioning

confidence: 67%

Effects of streptozotocin diabetes and fasting on intracellular sodium and adenosine triphosphate in rat soleus muscle.

Moore¹,

Munford²,

Pillsworth³

1983

The Journal of Physiology

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SUMMARY1. The hypothesis that part of the insulin transduction system consists of a co-ordinated stimulation of the Na pump and of Na-H exchange by the hormone (Moore, 1981) requires that insulin plays a physiological role in the regulation of intracellular Na+. Moreover, this model predicts that in hypoinsulinaemic states, such as diabetes and fasting, intracellular pH and intracellular ATP levels would be depressed. The present study tests the hypothesis that in hypoinsulinaemic states intracellular Na+ is increased and intracellular ATP is decreased by measuring these parameters in soleus muscles removed from both diabetic and fasted rats.2. When rats were made diabetic by injection of streptozotocin (SZ) plasma insulin significantly decreased by 24 hr and plasma glucose and triglyceride levels increased.3. Intracellular Na+ was significantly elevated by 48 hr after injection of SZ. The elevation ranged from 18 to 48 % and persisted for the duration of the experimental observation (up to 28 days).4. Intracellular ATP decreased significantly by the seventh day after SZ injection and remained depressed by about 24 % for the duration (35 days) of the observation.5. In one series, a significant negative correlation was seen between plasma insulin levels and intracellular Na+ of both SZ-diabetic animals and their controls.6. Intracellular Na+ also significantly increased when hypoinsulinaemia was induced by fasting.7. Again, intracellular ATP did not decrease until after the elevation ofintracellular Na+. After 72 hr of fasting, intracellular ATP was still decreased in spite of normal plasma glucose levels. 8. Insulin therapy of SZ diabetic rats restored intracellular ATP and plasma glucose to normal, but did not restore intracellular Na+ to normal levels.9. The results confirm two predictions of the 'insulin transduction system model (Moore, 1981). Most strongly supported is that part of the model which indicates that the Na pump is regulated by physiological levels of insulin. This is especially convincing since hypoinsulinaemia produced by a non-pharmacological procedure, fasting, was associated with an increase in intracellular Na+.

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“…muscle activity), which can enhance Na+ flux into muscle by neurotransmitter release or by decreased activity of membrane Na+-K+ ATPase, has been reported to decrease the concentration of NT-methylhistidine in human muscles (Rennie et al, 1981) and to decrease its release by perfused rat muscle subjected to electrical stimulation (Bylund-Fellenius et al, 1984). Diabetes has also been shown to decrease Na+-K+ ATPase activity and to increase intracellular Na+ in skeletal muscle, as well as in neural tissue, from rats (Moore et al, 1979;Greene & Lattimer, 1986;MacGregor & Matschinsky, 1986); furthermore, myofibrillar proteolysis is diminished in skeletal muscle from diabetic rats (Goodman, 1987a). Myofibrillar proteolysis has been reported to decrease during prolonged starvation in both humans (Young et al, 1973) and animals (Lowell et al, 1986b).…”

Section: Modulation Of Myofibriliar Proteolysis By Na+ or Activation mentioning

confidence: 99%

Acute alterations in sodium flux in vitro lead to decreased myofibrillar protein breakdown in rat skeletal muscle

Goodman

1987

Biochemical Journal

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Myofibrillar protein breakdown was evaluated by measuring the release of N tau-methylhistidine by isolated rat skeletal muscles or perfused rat muscles in the presence of a variety of agents known to affect Na+ flux. Total cell proteolysis was evaluated simultaneously by measuring tyrosine release by muscles after the inhibition of protein synthesis with cycloheximide. Treatment of muscles with the Na+ ionophore monensin or inhibitors of Na+-K+ ATPase (ouabain, digoxin or vanadate) decreased N tau-methylhistidine release by muscles by 21-35%. A phorbol ester (phorbol 12-myristate 13-acetate) as well as a synthetic diacylglycerol known to activate protein kinase C and a Na+/H+ antiport also decreased N tau-methylhistidine release by muscles. Removal of extracellular Na+ blocked the ability of these agents to attenuate N tau-methylhistidine release by muscles, suggesting that their effectiveness required a change in Na+ flux. In contrast with N tau-methylhistidine release by muscles, these agents, except for monensin, did not effect the release of tyrosine, suggesting that they attenuate specifically the breakdown of myofibrillar proteins. Overall these results indicate a link between Na+ and the regulation of protein breakdown in rat skeletal muscle, whereby an influx of Na+ can result in a decrease in myofibrillar proteolysis. Left unresolved is whether phospholipid hydrolysis is involved in this scheme.

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Effect of streptozotocin‐induced diabetes upon intracellular sodium in rat skeletal muscle

Cited by 17 publications

References 18 publications

Modifications induced by diabetes on the physicochemical and functional properties of erythrocyte plasma membrane

Modifications induced by diabetes on the physicochemical and functional properties of erythrocyte plasma membrane

Effects of streptozotocin diabetes and fasting on intracellular sodium and adenosine triphosphate in rat soleus muscle.

Acute alterations in sodium flux in vitro lead to decreased myofibrillar protein breakdown in rat skeletal muscle

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