Peripheral nerve abnormalities in the diabetic mutant mouse.
Observations were made on the genetically diabetic C57BL/Ks (db/db) mouse. Morphometric observations were performed on the tibial nerve at 6, 9, and 15 mo and compared with those from nondiabetic (m/m) controls. Myelinated fiber size was less in the diabetic animals at all stages and affected cross-sectional axon area and myelin thickness equally. Unmyelinated axons were unaffected. The index of circularity of myelinated axons did not differ between diabetic and control animals. No definite absolute reduction in fiber size occurred and degenerative changes, which were slight, were equally frequent in the diabetic and control nerves. Axonal glycogenosomes, polyglucosan particles, and Schwann cell/axon networks, and Schwann cell Reich granules increased with age in both groups, but only glycogenosomes were consistently more numerous in the diabetic animals. Counts of membrane associated particles in both P and E faces revealed that these were reduced in number in the diabetic animals in myelin and in axolemma of unmyelinated axons, but not in the axolemma of myelinated fibers. Growth in tibial length was also reduced in the diabetic animals and this suggested that the reduced fiber diameter probably represented a maturational deficit. The absence of a selective reduction in axonal size did not favor a primary axonopathy as the cause.
D000818:Animals; D001369:Axons / Q000648:ultrastructure; D003593:Cytoplasm / Q000648:ultrastructure; D003920:Diabetes Mellitus / Q000235:genetics* / Q000473:pathology; D005614:Freeze Fracturing; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009186:Myelin Sheath / Q000473:pathology; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D012583:Schwann Cells / Q000648:ultrastructure; D013979:Tibial Nerve / Q000473:pathology*