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Titolo:
Effect of sorbitol dehydrogenase inhibition on experimental diabetic autonomic neuropathy
Autore:
Schmidt, RE; Dorsey, DA; Beaudet, LN; Plurad, SB; Williamson, JR; Ido, Y;
Indirizzi:
WashingtonUSAiv, Sch Med, Dept Pathol, Div Neuropathol, St Louis, MO 63110Washington Univ St Louis MO USA 63110 Div Neuropathol, St Louis, MO 63110 WashingtonUSAiv, Sch Med, Dept Pathol, Div Anat Pathol, St Louis, MO 63110Washington Univ St Louis MO USA 63110 Div Anat Pathol, St Louis, MO 63110
Titolo Testata:
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
fascicolo: 12, volume: 57, anno: 1998,
pagine: 1175 - 1189
SICI:
0022-3069(199812)57:12<1175:EOSDIO>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALDOSE REDUCTASE INHIBITOR; NERVE GROWTH-FACTOR; DIETARY MYOINOSITOL SUPPLEMENTATION; RETROGRADE AXONAL-TRANSPORT; RAT SCIATIC-NERVE; NEUROAXONAL DYSTROPHY; PERIPHERAL-NERVE; ADENOSINE-TRIPHOSPHATASE; SYMPATHETIC-GANGLIA; CONDUCTION-VELOCITY;
Keywords:
diabetic neuropathy; neuroaxonal dystrophy; sorbitol dehydrogenase; sympathetic;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
69
Recensione:
Indirizzi per estratti:
Indirizzo: Schmidt, RE WashingtontUniv, Sch Med, Dept Pathol, Div Neuropathol, 660 S Euclid Ave, S Washington Univ 660 S Euclid Ave St Louis MO USA 63110 Ave, S
Citazione:
R.E. Schmidt et al., "Effect of sorbitol dehydrogenase inhibition on experimental diabetic autonomic neuropathy", J NE EXP NE, 57(12), 1998, pp. 1175-1189

Abstract

The polyol pathway and its dependent biochemical pathways are thought to play a role in the pathogenesis of diabetic neuropathy. We have developed ananimal model of diabetic autonomic neuropathy characterized by neuroaxonaldystrophy involving ileal mesenteric nerves and prevertebral sympathetic superior mesenteric ganglia (SMG) in chronic streptozocin-diabetic rats. Ourprevious studies have shown a salutary effect of aldose reductase inhibitors on experimental autonomic neuropathy, suggesting a role for the polyol pathway in its pathogenesis. In the current studies we have examined the effect of the sorbitol dehydrogenase inhibitor (SDI) CP-166,572, which interrupts the conversion of sorbitol to fructose (and reactions dependent on the second step of the polyol pathway) resulting in markedly increased levels of sorbitol in peripheral nerve. Fourteen weeks of treatment with CP-166,572resulted in a dramatically increased frequency of neuroaxonal dystrophy inileal mesenteric nerves and SMG. Although lesions developed prematurely and in greater numbers in SDI-treated diabetics than untreated diabetics did,their anatomic distribution and ultrastructural appearance were identical to that previously reported in long-term untreated diabetics. CP-166,572 treatment did not produce neuroaxonal dystrophy in control animals despite the fact that sciatic nerve sorbitol levels were markedly increased, reachingthe same levels as untreated diabetic animals. Treatment of diabetic rats for 14 weeks with the aldose reductase inhibitor zopolrestat resulted in a significant decrease in the frequency of neuroaxonal dystrophy compared with untreated diabetics.

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Documento generato il 30/10/20 alle ore 08:46:11