Prevention of defects of axonal transport in experimental diabetes by aldose reductase inhibitors.
Experiments on streptozotocin-diabetic rats have indicated that axonal transport of choline acetyltransferase is reduced in sciatic nerve. Treatment with an aldose reductase inhibitor both prevented and reversed this defect which was related to marked accumulations of sorbitol and fructose. Concurrent with these accumulations the content of myo-inositol in diabetic peripheral nerve is depleted. Further experiments taking account of nerve water content showed that the depletion of myo-inositol was 'real' not apparent. When the level of myo-inositol was maintained, either by feeding myo-inositol or by the inhibition of aldose reductase, the development of defective axonal transport of choline acetyltransferase and choline-containing lipids was prevented.
D000449:Aldehyde Reductase / Q000037:antagonists & inhibitors*; D000818:Animals; D001370:Axonal Transport / Q000187:drug effects*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D003929:Diabetic Neuropathies / Q000378:metabolism / Q000517:prevention & control*; D007294:Inositol / Q000172:deficiency; D013401:Sugar Alcohol Dehydrogenases / Q000037:antagonists & inhibitors*
D007294:Inositol; D013401:Sugar Alcohol Dehydrogenases; D000449:Aldehyde Reductase; D002795:Choline O-Acetyltransferase