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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 34 (1991), S. 387-389 
    ISSN: 1432-0428
    Keywords: Diabetes ; glycation ; tubulin ; microtubule ; sciatic nerve ; brain ; axonal transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetic neuropathy is associated with some early defects of axonal transport in experimental animals. Axonal transport is dependent on intact microtubules, and unsubstituted lysine residues of tubulin are essential for microtubule polymerization. As lysine residues are the major target for the non-enzymatic attachment of glucose, the effect of diabetes on the extent of glycation of tubulin was investigated. There was a more than four-fold increase in the extent of glycation of tubulin in the sciatic nerve of rats with streptozotocin-induced diabetes of 2 weeks duration compared with control rats. In contrast, no such increase in glycation was observed in brain microtubule protein from diabetic rats at that stage of diabetes. Incubation of brain microtubule protein with glucose prior to in vitro polymerization showed that the early stages of glycation were not associated with inhibition of microtubule assembly. The observed glycation of peripheral nerve tubulin in early experimental diabetes may nevertheless contribute to axonal transport abnormalities through an as yet undetermined impairment of microtubule function.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Streptozotocin ; diabetes mellitus ; nerve regeneration ; ornithine decarboxylase ; neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ornithine decarboxylase activity was measured in the dorsal root ganglia from crushed and uncrushed contralateral sciatic nerve of control and streptozotocin-diabetic rats. A further group of diabetic rats was treated with insulin throughout the experiment. Ornithine decarboxylase activity in ganglia from uncrushed nerves was the same in diabetic and non-diabetic rats. A significant (greater than 4-fold) increase in mean levels of ornithine decarboxylase activity 72 h after crush injury was found in ganglia from crushed nerves in non-diabetic but not in diabetic rats. The enzyme activity in ganglia from diabetic rats treated with insulin resembled that in non-diabetic rats. Twenty-four hours after crush injury, ornithine decarboxylase activity in ganglia from crushed nerves was higher in non-diabetic than in diabetic animals. This may be responsible for the delayed and defective nerve regeneration known to occur in peripheral nerve of the streptozotocin-diabetic rat.
    Type of Medium: Electronic Resource
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