Histopathological heterogeneity of neuropathy in insulin-dependent and non-insulin-dependent diabetes, and demonstration of axo-glial dysjunction in human diabetic neuropathy.

摘要: Abstract Altered sorbitol and myo-inositol metabolism, (Na,K)-ATPase function, electrochemical sodium gradients, axonal swelling, distortion disruption of the node Ranvier ("axo-glial dysjunction") directly implicate hyperglycemia in pathogenesis neuropathy diabetic rats, but relevance this sequence to clinical heterogeneous groups patients remains be established. Fascicular sural nerve morphometry 11 with complicating insulin-dependent diabetes revealed a pattern interrelated structural changes strikingly similar that rat when compared age-matched controls. 17 older non-insulin-dependent comparable duration severity neuropathy, displayed fiber loss, paranodal demyelination, remyelination segmental demyelination controls, axo-glial dysjunction was replaced by Wallerian degeneration as primary manifestation damage, loss occurred spatial consistent an ischemic component. The mechanistic model developed from does indeed appear apply human superimposed hormonal, metabolic, vascular, and/or age-related effects alter morphologic expression non-insulin dependent diabetes.