Peripheral neuropathy in mouse hereditary diabetes mellitus. II. Ultrastructural correlates of degenerative and regenerative changes.

Published

Journal Article

The fine structural changes in some peripheral nerves and sensory ganglia from mice (C57BL/KsJ, db/db) with an hereditary diabetic syndrome, similar to human maturity-onset diabetes mellitus, were studied during development of the mild peripheral neuropathy. The abnormalities observed included axonal degeneration, disruption of myelin, accumulation of electro-dense material in axons, satellite cells and Schwann cells, increased frequency of pi granules of Reich in Schwann cells, enlarged mitochondria, and proliferated and thickened Schwann cell basal laminae. Distal hind limb nerves were most affected. Sensory ganglion neurons were normal except for occasional chromatolytic cells, so that nerve cell loss was not present in this peripheral neuropathy. Morphological indications of Schwann cell hyperplasia, hypertrophy, and axonal sprouting supported the contention that a continuous cycle of axonal degeneration and regeneration was occurring. The ultrastructural changes and accumulation of electron-opaque, lipid material suggested that a defect in lipid metabolism, secondary to the diabetic condition, could be an important factor in the peripheral neuropathy in the diabetic mouse.

Full Text

Duke Authors

Cited Authors

  • Carson, KA; Bossen, EH; Hanker, JS

Published Date

  • September 1, 1980

Published In

Volume / Issue

  • 6 / 5

Start / End Page

  • 361 - 374

PubMed ID

  • 6969863

Pubmed Central ID

  • 6969863

International Standard Serial Number (ISSN)

  • 0305-1846

Digital Object Identifier (DOI)

  • 10.1111/j.1365-2990.1980.tb00672.x

Language

  • eng

Conference Location

  • England