Morphometrical Analysis of the Peripheral Nerve Lesions in Experimental Diabetes Rats

Yagihashi, Soroku; Nishihira, Morimi; Baba, Masayuki

doi:10.1620/tjem.129.139

Cited by 17 publications

(7 citation statements)

References 9 publications

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“…The point about lamellar separation or splitting is more important. Rather than reitterate arguments already made in our paper [1], we quote from a recent study by Mattingly and Fischer [5] using streptozotocin-diabetic rats, whose findings are in good agreement with our own "... myelin abnormalities which could produce an increase in the size of the myelin sheath inculding delamination, splitting, wrinkling and notching have been observed by many investigators ..." [8,[11][12][13][14]. We did not think it was justifiable to exclude these badly affected areas or fibres from our sample, as to do so would have biased our estimate of myelin sheath area towards normality.…”

Section: Sirsupporting

confidence: 86%

Myelinated nerve fibres in experimental diabetes: a reply to Bhoyrul and Sharma

Cameron

Leonard

1986

Diabetologia

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Section: Sirsupporting

confidence: 86%

Myelinated nerve fibres in experimental diabetes: a reply to Bhoyrul and Sharma

Cameron

Leonard

1986

Diabetologia

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“…There is little doubt that chemically induced diabetes in the rat causes axonal degeneration accompanied by ultrastructural signs of sprouting and regeneration (20)(21)(22). These changes are said to be less marked in insulin-treated diabetic rats (23).…”

Section: Discussionmentioning

confidence: 99%

Deficient Axonal Transport of Substance P in Streptozocin-Induced Diabetic Rats: Effects of Sorbinil and Insulin

Tomlinson

Robinson²,

Willars³

et al. 1988

Diabetes

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This study measured the accumulation of substance P-like immunoreactivity (SPLI) proximal and distal to 12-h constricting ligatures applied to rat sciatic nerves. There were three separate experiments, and the baseline for each consisted of control and age-matched rats with 3 wk of untreated streptozocin-induced diabetes. We compared the effects of twice-daily insulin treatment, daily sorbinil (25 mg.kg-1.day-1 p.o.), and a combination of both treatments. In untreated diabetic rats the anterograde accumulation of SPLI was reduced by 30-40%. This deficit was unaffected by sorbinil alone but was attenuated by insulin and prevented completely by insulin and sorbinil combined. There were also indications that diabetes caused reductions in retrograde accumulation of SPLI and its content in unconstricted nerve and the L4 dorsal root ganglion. The fraction of SPLI undergoing net anterograde or retrograde movement and the velocities of accumulation were unaffected by diabetes or the treatment regimens. These findings indicate a reduction in the amount of substance P moved by axonal transport in diabetic rats that is related partly to aldose reductase activity and partly to some other insulin-correctable consequence of experimental diabetes.

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“…In both HDN and EDN there is thickening of the capillary wall, reduplication of membrane base-men~s,~~."6.41.42.45.~11,52.~4. 65 and evidence of capillary c l o~u r e .~~~~…”

Section: Evidence For Microvascular Abnormalitiesmentioning

confidence: 99%

Recent advances in the pathogenesis of diabetic neuropathy. Clues from human diabetic neuropathy

Low

1987

Muscle and Nerve

112

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Recent advances in the understanding of the pathogenesis of diabetic neuropathy have been made in six areas. There is support for the notion that a reduction in nerve free myoinositol may be responsible in part for the nerve conduction slowing in diabetic neuropathy. There is further evidence of microvascular abnormalities, including morphometric evidence of multifocal fiber loss and of capillary changes in biopsied sural nerve. There is evidence of endoneurial hypoxia, including the findings of reduced nerve blood flow and endoneurial oxygen tensions in chronic experimental diabetic neuropathy (EDN). The major mechanisms of resistance to ischemic conduction failure (RICF) is the marked increase in nerve energy substrates. Recent studies provide certain insights into clinical characteristics of human diabetic neuropathy (HDN), including the asymmetric pattern of HDN, the paradox between liability to pressure palsies and RICF, and insulin-related acute painful neuropathy. The suggested pathogenetic scheme incorporates the notion that once hypoxia is established, it may start a vicious cycle of further capillary damage and escalating hypoxia.

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Morphometrical Analysis of the Peripheral Nerve Lesions in Experimental Diabetes Rats

Cited by 17 publications

References 9 publications

Myelinated nerve fibres in experimental diabetes: a reply to Bhoyrul and Sharma

Myelinated nerve fibres in experimental diabetes: a reply to Bhoyrul and Sharma

Deficient Axonal Transport of Substance P in Streptozocin-Induced Diabetic Rats: Effects of Sorbinil and Insulin

Recent advances in the pathogenesis of diabetic neuropathy. Clues from human diabetic neuropathy

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