K. Sugimoto et al., Peripheral nerve structure and function in long-term galactosemic dogs: morphometric and electron microscopic analyses, ACT NEUROP, 97(4), 1999, pp. 369-376
Experimental galactosemia for activating the polyol pathway is used extensi
vely to explore the pathogenesis of diabetic complications. However, despit
e the presence of severe neuropathy in galactosemic rats, changes in the pe
ripheral nerve have not been well established in galactosemic dogs. We ther
efore conducted biochemical, electrophysiological, and morphometric studies
on peripheral nervous systems (PNS) in dogs given a 30% galactose diet for
44 months. Age- and sex-matched dogs given a 30% cellulose diet were used
as control. Chronic galactosemia resulted in accumulation of galactitol and
decrease in myo-inositol in the sciatic nerve. Electrophysiological and te
ased fiber analyses demonstrated no significant abnormalities in the ulnar
and peroneal nerves in galactosemic dogs. Morphometric analyses revealed a
tendency of myelinated fiber atrophy (24% reduction of average fiber size)
associated with 20% decrease (P < 0.05 vs control) in mean myelinated fiber
occupancy rate in the peroneal nerve in galactosemic dogs. In the anterior
mesenteric ganglion, there was a slight but significant increase (8%) in m
ean neuronal cell size in galactosemic dogs (P < 0.05 vs control). Electron
microscopy revealed that galactosemia did not produce dystrophic and degen
erative changes in the autonomic ganglion in dogs. We conclude that structu
ral and functional changes in the PNS of galactosemic dogs are mild and dif
ferent from those of the rat model. These findings suggest that the severit
y of peripheral neuropathy induced by chronic galactosemia may be species d
ependent.