Mechanism of glucose-induced (Na+, K+)-ATPase inhibition in aortic wall of rabbits

@article{Simmons2004MechanismOG,
  title={Mechanism of glucose-induced (Na+, K+)-ATPase inhibition in aortic wall of rabbits},
  author={D. A. Simmons and Albert I. Winegrad},
  journal={Diabetologia},
  year={2004},
  volume={32},
  pages={402-408}
}
SummaryHyperglycaemia decreases (Na+, K+)-ATPase activity in specific tissues by a mechanism whose effects are prevented by aldose reductase inhibitors and by raising plasma myo-inositol. This mechanism was activated and studied in vitro in normal rabbit aortic intima-media. Raising medium glucose to 10 mmol/l for 60 min inhibited a major component of (Na+, K+)-ATPase-mediated 86Rb + /K+ uptake normally operative in resting aortic intima-media in medium containing normal plasma levels of… Expand
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References

SHOWING 1-10 OF 32 REFERENCES
Insulin stimulation of (Na+,K+)-adenosine triphosphatase-dependent 86Rb+ uptake in rat adipocytes.
TLDR
It is concluded that the uptake of 86Rb+ by the (Na+,K+)-ATPase is an insulin-sensitive membrane transport process in the fat cell. Expand
Basal phosphatidylinositol turnover controls aortic Na+/K+ ATPase activity.
TLDR
Depleting endogenous free AA with medium defatted albumin selectively inhibits the component of basal de novo PI synthesis that replenishes the rapidly turning-over PI pool. Expand
Effects of elevated glucose concentrations on the metabolism of the aortic wall.
TLDR
The effects of elevated glucose concentrations on the metabolism of the aortic wall were examined in a preparation of tubular segments of rabbit descending thoracic aorta comprised of intima and media only, suggesting that elevated ambient glucose concentrations result in significant alterations in the metabolism in aorto- media. Expand
Sorbitol, phosphoinositides, and sodium-potassium-ATPase in the pathogenesis of diabetic complications.
TLDR
Aldose reductase inhibitors firmly link defects in myo-inositol metabolism to activation of the polyol pathway in diabetes; the resulting "sorbitol-myo- inositol hypothesis" has been extended from its application to the lenses and peripheral nerves to most of the tissues involved with diabetic complications. Expand
Myo-inositol and sorbitol metabolism in relation to peripheral nerve function in experimental diabetes in the rat: The effect of aldose reductase inhibition
TLDR
Both sorbinil and myo-inositol treatment partially reversed the slowing of motor-nerve conduction velocity in diabetic rats, which was discussed in relation to the involvement of sorbitol andMyo- inositol metabolism in the aetiology of diabetic neuropathy. Expand
Myo-inositol transport in plamsa membrane of rat kidney.
TLDR
The results indicate that the plasma membrane of rat kidney has a cyclitol carrier system specific to myo -inositol and scyllitol, which represents the entry into the intravesicular spaces rather than binding to the membrane. Expand
Studies of the Effects of an Elevated Glucose Concentration on the Ultrastructure and Composite Metabolism of the Intact Rabbit Aortic Intima-Media Preparation
TLDR
Ambient glucose concentration is not the primary determinant of composite-free intracellular glucose concentration in arterial wall, and an increase in medium glucose concentration does not result in a significant increase in glucose utilization via the polyol pathway or induce the concomitants of increasedpolyol pathway activity demonstrable in a conventionally prepared aortic intima-media preparation. Expand
Aldose reductase, glomerular metabolism, and diabetic nephropathy.
  • M. Cohen
  • Chemistry, Medicine
  • Metabolism: clinical and experimental
  • 1986
TLDR
It is found that glomerular polyol content is significantly increased in diabetes, whereasglomerular myo-inositol content are significantly reduced and the ability of sorbinil to impact on these changes suggests that it could favorably impact on the nephropathic process. Expand
Impaired rat sciatic nerve sodium-potassium adenosine triphosphatase in acute streptozocin diabetes and its correction by dietary myo-inositol supplementation.
TLDR
In diabetic peripheral nerve, abnormal myo-inositol metabolism is associated with abnormal sodium-potassium ATPase activity, and the mechanism of the effect of dietary myo, inositol to correct diabetic nerve conduction may be through changes in a Sodium-pot potassium ATPase, possibly via changes in myO-inotol-containing phospholipids. Expand
Significance of tissue myo-inositol concentrations in metabolic regulation in nerve.
Approximately 25 percent of resting energy utilization in isolated nerve endoneurium is inhibited by medium containing defatted albumin and selectively restored by arachidonic acid but is unaffectedExpand
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