Sorbitol Pathway: Presence in Nerve and Cord with Substrate Accumulation in Diabetes

  title={Sorbitol Pathway: Presence in Nerve and Cord with Substrate Accumulation in Diabetes},
  author={Kenneth H. Gabbay and Lorenzo O. Merola and Richard A. Field},
  pages={209 - 210}
Glucose, sorbitol, fructose, and inositol are present in peripheral nerve and spinal cord. Marked elevation of these substances occurs in these tissues in mildly diabetic animals. These alterations provide biochemical mechanisms which could be significant in the etiology of diabetic neuropathy. 
Sorbitol, inositol and nerve conduction in diabetes.
Treatment with the aldose reductase inhibitor Sorbinil restored motor nerve conduction velocity to normal in streptozotocin-diabetic rats and genetically diabetic mice and corrected defects in inositol and sorbitol in sciatic nerve. Expand
Aldose reductase inhibitors: pharmacological data and therapeutic perspectives
Abstract The activation of the ‘polyol pathway' in diabetes, inducing an accumulation of sorbitol in peripheral nerve, is an important factor in the pathogenesis of diabetic polyneuritis. InhibitorsExpand
Nerve glucose, fructose, sorbitol, myo-inositol, and fiber degeneration and regeneration in diabetic neuropathy.
The results indicate that myo-inositol deficiency is not part of the pathogenesis of human diabetic neuropathy, as had been hypothesized and other accumulated alcohol sugars, however, were increased in diabetes and were associated with the severity of neuropathy. Expand
Effect of Blood Sugar Control on the Accumulation of Sorbitol and Fructose in Nervous Tissues
It is found that accumulation in nerves of the products of the sorbitol pathway may be minimized when blood sugar is controlled, and it is postulated that herein lies the mechanism whereby control of diabetes is likely to lead to a reduction in the incidence of nerve damage. Expand
Lipid synthesis in peripheral nerve from alloxan diabetic rats
A change in the type of cerebrosides synthesized is seen with a pronounced decrease in the rate of incorporation of saturated fatty acids, and Cerebroside synthesis is more depressed than that of any other fraction. Expand
Aldose reductase inhibitors and diabetic complications.
In experimental models there is proof of activity against biochemical, functional and structural defects in all of the involved tissues, but it is awaited full clinical verification of this potential. Expand
Prevention of Neural Myoinositol Depletion in Diabetic Rats by Aldose Reductase Inhibition with Tolrestat 1
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  • 1986
Tolrestat completely prevented the accumulation of sorbitol and the depletion of myoinositol in male Wistar and Sprague-Dawley rats rendered diabetic with streptozocin. Expand
The sorbitol pathway and the complications of diabetes.
  • K. Gabbay
  • Medicine
  • The New England journal of medicine
  • 1973
The main problems in the care of diabetic patients are ketoacidosis and infections, but since the introduction of insulin therapy, these problems are no longer the main problems. Expand
Nerve Conduction Defect in Galactose-fed Rats
Findings suggest that the accumulation of sugar alcohol plays an important role in the etiology of galactosemic neuropathy. Expand
Glucose utilization by the polyol pathway in human erythrocytes.
Sorbitol is present in human erythrocytes in concentrations exceeding that in plasma, and is linearly related to the plasma glucose concentration, and appears to be a physiological substrate for alditol:NADP oxidoreductase in the ERYthrocyte. Expand


Identification of fructose in mammalian nerve
The presence of substantial levels of fructose in peripheral nerve and lower levels in brain is reported, suggesting that fructose may originate from glucose via sorbitol and be present in nervous tissue. Expand
Osmotic changes in experimental galactose cataracts.
Evidence has been presented indicating that when galactose is made available to the lens, either by feeding experiments, or by in vitro incubation, there is an accumulation of dulcitol, and the resulting increase in water volume may be sufficient to cause the lens fibres to swell and perhaps to rupture their membranes. Expand
Non-glycolytic Pathways of Metabolism of Glucose.
Kinoshita for his interest and encouragement in this project. Supported in part by PHS grants NB-04063-04 and TI AM 5072