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Ganglioside Treatment of Streptozotocin‐Diabetic Rats Prevents Defective Axonal Transport of 6‐Phosphofructokinase Activity
Author(s) -
Calcutt N. A.,
Tomlinson D. R.,
Willars G. B.
Publication year - 1988
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1988.tb03033.x
Subject(s) - endocrinology , medicine , ganglioside , phosphofructokinase , sciatic nerve , streptozotocin , axon , chemistry , diabetes mellitus , creatine kinase , diabetic neuropathy , nerve conduction velocity , biology , glycolysis , biochemistry , anatomy , metabolism
This study measured axonal transport of 6‐phosphofructokinase (PFK) and aldolase activities in the sciatic nerves of rats with short‐term streptozotocin‐induced diabetes. The diabetic rats showed deficits in anterograde (69% of controls; p < 0.001) and retrograde (33% of controls; p < 0.01) accumulations of PFK activity as well as its content per unit length of unconstricted sciatic nerve (86% of controls; p < 0.05). There were no accumulation deficits in aldolase activity in the nerves of the diabetic rats, although the activity per unit length of unconstricted nerve was deficient (81% of controls; p < 0.05). Treatment of diabetic rats with mixed bovine brain gangliosides (10 mg/kg of body weight/day, i.p.) did not affect the deficit in PFK activity in unconstricted nerve (84% of ganglioside‐treated controls; p < 0.01), but all the other defects in enzyme activities were prevented completely. The diabetic rats also showed a reduction of 7% (p < 0.01) in sciatic nerve dry weight per unit length, which was prevented by ganglioside treatment. In contrast, the reduced motor nerve conduction velocity, accumulation of polyol pathway metabolites, and depletion of myo ‐inositol. characteristic of untreated short‐term diabetes, were unaffected by ganglioside treatment.