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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 19 (1980), S. 222-228 
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; axonal transport ; Streptozotocin diabetes ; nerve crush ; nerve regeneration ; insulin treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The axonal transport of proteins in crushed nerves of streptozotocin (40 mg/kg) diabetic rats was investigated 4 weeks after induction of diabetes. 35S-methionine was used as a marker for protein and 3H-fucose as a marker for glycoprotein. The precursors were injected into the fifth lumbar spinal ganglion and the accumulation of TCA-insoluble activity proximal and distal to a sciatic nerve ligature was measured at different time intervals after application of a crush. The start of accumulation distal to the ligature was delayed by 1 hour for proteins as well as for glycoproteins. Furthermore, the total amount of accumulated protein after 19 h was decreased by 18% while the decrease was 21% for glycoprotein. By insulin treatment the differences could both be prevented and reversed after 3 days of normoglycaemia. These findings demonstrate an impaired response to a nerve crush and might be the explanation for the regenerative abnormalities of peripheral nerves in diabetes.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 20 (1981), S. 110-112 
    ISSN: 1432-0428
    Keywords: Axonal transport ; diabetic neuropathies ; streptozotocin diabetes ; nerve crush
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The accumulation of 3H-fucose labelled glycoprotein and 35S-methionine labelled protein carried by the retrograde axonal transport in the sensory fibres of the sciatic nerve was examined on the day after injection of streptozotocin in rats. The accumulation of fucose-label was reduced (2.8 ± 0.4 (SD) versus 2.1 ± 0.5 (arbitrary units), 2p = 0.0044) indicating a decreased retrograde flux of glycoproteins. This early transport abnormality could have a key role in the development of peripheral neuropathy in diabetes.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 19 (1980), S. 229-233 
    ISSN: 1432-0428
    Keywords: Galactose-feeding ; axonal transport ; diabetic neuropathies ; nerve crush
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Axonal transport was studied in galactosefed rats. Precursors for proteins and glycoproteins were injected into the fifth lumbar spinal ganglion and retrograde axonal transport as well as slow axonal transport were estimated at different time intervals during the following 4 weeks. Galactose-feeding was found to produce a progressive reduction of the retrograde axonal transport of glycoproteins in intact nerve (2.9±0.2 (arbitrary units) after five days of galactose-feeding as compared to 1.9±0.7 after 28 days, 2p=0.025). The slow axonal transport velocity of structural proteins was reduced from 0.97 ±0.09 mm/day to 0.84±0.04 mm/day, 2p=0.0030. The present findings as well as structural and electrophysiological abnormalities of the nerves of galactose-fed rats are similar to the changes found in diabetic rats. The similarities point to a decisive role for glucose or its metabolites in the development of diabetic neuropathy.
    Type of Medium: Electronic Resource
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