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Axonal transport of choline acetyltransferase and 6‐phosphofructokinase activities in genetically diabetic mice
Author(s) -
Calcutt Nigel A.,
Willars Gary B.,
Tomlinson David R.
Publication year - 1988
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880111204
Subject(s) - choline acetyltransferase , phosphofructokinase , genetically modified organism , genetically engineered , endocrinology , medicine , biology , chemistry , biochemistry , enzyme , glycolysis , gene , acetylcholine
This study examined the anterograde axonal transport of activities of the cytoplasmic enzymes choline acetyltransferase and 6‐phosphofructokinase in genetically diabetic C57BL/Ks (db/db) mice and their nondiabetic (+/?) littermates. Diabetic mice exhibited marked reductions in the accumulation of both choline acetyltransferase and 6‐phosphofructokinase activity against a constriction of the left sciatic nerve (38% and 51% of nondiabetic values, respectively). Enzyme activities per unit length of unconstricted nerve were not different from those of nondiabetic mice. The nerves of diabetic mice did not accumulate measurable amounts of sorbitol or fructose and showed no myo‐inositol depletion. Thus this study concludes that, in diabetic mice, the deficits in anterograde axonal transport of these two enzymes do not arise from the accumulation of sorbitol and fructose nor from depletion of nerve free myo‐inositol.