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Diabetes, Vol 36, Issue 12 1425-1431, Copyright © 1987 by American Diabetes Association

ARTICLES

Does galactose feeding provide a valid model of consequences of exaggerated polyol-pathway flux in peripheral nerve in experimental diabetes?

GB Willars, JE Lambourne and DR Tomlinson
Department of Physiology and Pharmacology, Medical School, Queens Medical Centre, Nottingham, United Kingdom.

This study was designed to examine the effect of exaggerated polyol-pathway flux on sciatic nerve content of polyols, myo-inositol, and water. Rats with streptozocin-induced diabetes of 3- and 12-wk duration and nondiabetic rats fed for 5 days on a diet containing 20% galactose were employed initially. All three conditions showed marked elevation of nerve polyol content, combined with fructose accumulation in the diabetic rats. Galactose-fed rats showed a significant (P less than .01) increase in nerve water content of approximately 30% (when expressed as water/unit dry wt tissue). Diabetic rats showed no change in nerve water. Both diabetic and galactose-fed rats showed a depletion of nerve free myo-inositol, although the extent of depletion was greater in the latter. All these changes were prevented or attenuated by the aldose reductase inhibitor Statil (ICI 128436). When diabetic rats were fed a 20% galactose diet for 5 days, nerves of 3- but not 12-wk diabetic rats showed marked increases in water content. A more mild degree of galactosemia, induced by 5 or 21 days of feeding a diet containing 10% galactose to nondiabetic rats, provoked an increase in nerve water content associated with polyol levels of a similar order to those seen in diabetes. We do not know why polyol-pathway metabolites cause nerve hyperhydration in galactosemia but not in streptozocin-induced diabetes. Such differences urge caution in the use of galactose feeding to model the consequences of exaggerated polyol-pathway flux in nerve to face questions related to neuronal dysfunction in diabetes.
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Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1987 by the American Diabetes Association.