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Titolo:
Inhibition of sorbitol dehydrogenase exacerbates autonomic neuropathy in rats with streptozotocin-induced diabetes
Autore:
Schmidt, RE; Dorsey, DA; Beaudet, LN; Plurad, SB; Parvin, CA; Yarasheski, KE; Smith, SR; Lang, HJ; Williamson, JR; Ido, Y;
Indirizzi:
Washington Univ, Sch Med, Dept Pathol & Immunol, Div Neuropathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Neuropathol, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Lab Med, Div Neuropathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Neuropathol, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Internal Med, Div Neuropathol, St Louis, MO63110 USA Washington Univ St Louis MO USA 63110 Neuropathol, St Louis, MO63110 USA Washington Univ, Sch Med, Dept Anat Pathol, Div Neuropathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Neuropathol, St Louis, MO 63110 USA Aventis Pharma Deutschland GMBH, Chem Res Frankfurt, Frankfurt, Germany Aventis Pharma Deutschland GMBH Frankfurt Germany t, Frankfurt, Germany
Titolo Testata:
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
fascicolo: 12, volume: 60, anno: 2001,
pagine: 1153 - 1169
SICI:
0022-3069(200112)60:12<1153:IOSDEA>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALDOSE REDUCTASE INHIBITOR; SYMPATHETIC-GANGLIA; NEUROAXONAL DYSTROPHY; NERVE-CONDUCTION; ELEVATED GLUCOSE; MYOINOSITOL; METABOLISM; PATHWAY; SENSITIVITY; INNERVATION;
Keywords:
diabetic neuropathy; sorbitol pathway; sympathetic neuroaxonal dystrophy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Schmidt, RE Washington Univ, Sch Med, Dept Pathol & Immunol, Div Neuropathol, 660 S Euclid Ave, St Louis, MO 63110 USA Washington Univ 660 S Euclid Ave St Louis MO USA 63110 110 USA
Citazione:
R.E. Schmidt et al., "Inhibition of sorbitol dehydrogenase exacerbates autonomic neuropathy in rats with streptozotocin-induced diabetes", J NE EXP NE, 60(12), 2001, pp. 1153-1169

Abstract

We have developed an animal model of diabetic autonomic neuropathy that ischaracterized by neuroaxonal dystrophy (NAD) involving ileal mesenteric nerves and prevertebral sympathetic superior mesenteric ganglia (SMG) in chronic streptozotocin (STZ)-diabetic rats. Studies with the sorbitol dehydrogenase inhibitor SDI-158, which interrupts the conversion of sorbitol to fructose (and reactions dependent on the second step of the sorbitol pathway), have shown a dramatically increased frequency of NAD in ileal mesenteric nerves and SMG of SDI-treated versus untreated diabetics. Although lesions developed prematurely and in greater numbers in SDI-treated diabetics, their distinctive ultrastructural appearance was identical to that previously reported in long-term untreated diabetics. An SDI effect was first demonstrated in the SMG of rats that were diabetic for as little as 5 wk and was maintained for at least 7.5 months. As in untreated diabetic rats, rats treated with SDI i) showed involvement of lengthy ileal, but not shorter, jejunal mesenteric nerves; ii) demonstrated NAD in paravascular mesenteric nerves distributed to myenteric gan.-Iia while sparing adjacent perivascular axons ramifying within the vascular adventitia; and, iii) failed to develop NAD inthe superior cervical ganglia (SCG). After only 2 months of SDI-treatment,tyrosine hydroxylase immunolocalization demonstrated marked dilatation of postganglionic noradrenergic axons in paravascular ileal mesenteric nerves and within the gut wall versus those innervating extramural mesenteric vasculature. The effect of SDI on diabetic NAD in SMG was completely prevented by concomitant administration of the aldose reductase inhibitor Sorbinil. Treatment of diabetic rats with Sorbinil also prevented NAD in diabetic ratsnot treated with SDI. These findings indicate that sorbitol pathway-linkedmetabolic imbalances play a critical role in the development of NAD in this model of diabetic sympathetic autonomic neuropathy.

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Documento generato il 30/10/20 alle ore 23:56:17