Delayed Wallerian degeneration and increased neurofilament phosphorylation in sciatic nerves of rats with streptozocin-induced diabetes

Terada, Masahiko; Yasuda, Hitoshi; Kikkawa, Ryuichi

doi:10.1016/s0022-510x(97)00269-4

Cited by 57 publications

(49 citation statements)

References 29 publications

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“…Diabetic rats have impaired nerve regeneration, and previous studies have shown impaired macrophage recruitment, albeit at a number of weeks after injury (38,39). In the present study, there was a trend toward fewer endoneurial macrophages in diabetic nerves 7 days after nerve crush, which might be the precursor to the deficit in macrophage recruitment seen at later time points by others.…”

Section: Discussionsupporting

confidence: 62%

Ciliary Neurotrophic Factor Improves Nerve Conduction and Ameliorates Regeneration Deficits in Diabetic Rats

Mizisin

Shuff

et al. 2004

Diabetes

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Ciliary neurotrophic factor (CNTF) protein and bioactivity are reduced in the peripheral nerve of hyperglycemic rats with a cause related to metabolism of hexose sugars by aldose reductase. Here the efficacy of CNTF treatment against disorders of nerve function in hyperglycemic rats was investigated. CNTF treatment from the onset of 8 weeks of galactose feeding prevented nerve conduction slowing in a dose-dependent manner. Streptozotocin-induced diabetic rats were maintained for 4 weeks before CNTF treatment was initiated. Four weeks of CNTF treatment significantly improved nerve conduction compared with untreated diabetic rats and also normalized the recovery of toe spread after sciatic nerve crush. One week of CNTF treatment significantly improved the distance of sensory nerve regeneration achieved after nerve crush injury compared with untreated diabetic rats. CNTF was without effects on any parameter in nondiabetic rats. Eight weeks of diabetes did not impair macrophage recruitment 1 and 7 days after nerve crush; neither did intraneural injections of CNTF and CNTFR␣ enhance recruitment in diabetic or control rats. These observations point to the potential utility of CNTF in treating nerve dysfunction in experimental diabetes.

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Section: Discussionsupporting

confidence: 62%

Ciliary Neurotrophic Factor Improves Nerve Conduction and Ameliorates Regeneration Deficits in Diabetic Rats

Mizisin

Shuff

et al. 2004

Diabetes

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“…Regeneration was slowed after nerve injury in rat models of type 1 DM with alterations occurring in various components of the process. For example Wallerian degeneration, which is a precondition for normal regeneration following nerve injury, was delayed in the nerves of streptozotocin(STZ)-induced diabetic rats [14]. Both crush and transection of sciatic nerves in diabetic mice (STZ-induced) were followed by defective repopulation and maturation of axons [15], which was confirmed by various morphological and electrophysiological approaches.…”

Section: Problems With Nerve Regeneration In Diabetes Mellitusmentioning

confidence: 89%

Advanced Diabetic Neuropathy: A Point of no Return?

Bouc̆ek¹

2006

Rev Diabetic Stud

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■ AbstractDiabetic peripheral neuropathy is the most common complication of long-standing diabetes mellitus which frequently results in clinically significant morbidities e.g. pain, foot ulcers and amputations. During its natural course it progresses from initial functional changes to late, poorly reversible, structural changes. Various interconnected pathogenetic concepts of diabetic neuropathy have been proposed based on metabolic and vascular factors, mostly derived from long-term hyperglycemia. These pathogenetic mechanisms have been targeted in several experimental and clinical trials. This review summarizes available, mainly morphological data from interventions designed to halt the progression or achieve the reversal of established diabetic neuropathy, which include the recovery of normoglycemia by pancreas or islet transplantation, polyol pathway blockade by aldose reductase inhibitors, mitigation of oxidative stress by the use of antioxidants or correction of abnormalities in essential fatty acid metabolism. Unfortunately, to date, no treatment based on pathogenic considerations has shown clear positive effects and thus early institution of optimal glycemic control remains the only available measure with proven efficacy in preventing or halting progression of diabetic neuropathy. Further experimental and clinical research employing objective reproducible parameters is clearly needed. Novel noninvasive or minimally invasive methods e.g. corneal confocal microscopy or epidermal nerve fiber counts may represent potentially useful instruments for the objective assessment of nerve damage and monitoring of treatment effects.

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“…They interact with microtubules, thereby providing axonal transport. Several kinases are involved in NF phosphorylation, like the cyclin-dependent kinase Cdk5, the MAP kinases Erk ½, SAPK [81], and GSKβ [82,83].…”

Section: C-peptide and Axonal Atrophymentioning

confidence: 99%

The Beneficial Effects of C-Peptide on Diabetic Polyneuropathy

Kawanishi

Zhang²,

Sima³

2009

Rev Diabet Stud

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■ AbstractDiabetic polyneuropathy (DPN) is a common complication in diabetes. At present, there is no adequate treatment, and DPN is often debilitating for patients. It is a heterogeneous disorder and differs in type 1 and type 2 diabetes. An important underlying factor in type 1 DPN is insulin deficiency. Proinsulin C-peptide is a critical element in the cascade of events. In this review, we describe the physiological role of C-peptide and how it provides an insulin-like signaling function. Such effects translate into beneficial outcomes in early metabolic perturbations of neural Na + /K + -ATPase and nitric oxide (NO) with subsequent preventive effects on early nerve dysfunction. Further corrective consequences resulting from this signaling cascade have beneficial effects on gene regulation of early gene responses, neurotrophic factors, their receptors, and the insulin receptor itself. This may lead to preventive and corrective results to nerve fiber degeneration and loss, as well as, promotion of nerve fiber regeneration with respect to sensory somatic fibers and small nociceptive nerve fibers. A characteristic abnormality of type 1 DPN is nodal and paranodal degeneration with severe consequences for myelinated fiber function. This review deals in detail with the underlying insulin-deficiency-related molecular changes and their correction by C-peptide. Based on these observations, it is evident that continuous maintenance of insulin-like actions by C-peptide is needed in peripheral nerve to minimize the sequences of metabolic and molecular abnormalities, thereby ameliorating neuropathic complications. There is now ample evidence demonstrating that C-peptide replacement in type 1 diabetes promotes insulin action and signaling activities in a more enhanced, prolonged, and continuous fashion than does insulin alone. It is therefore necessary to replace C-peptide to physiological levels in diabetic patients. This will have substantial beneficial effects on type 1 DPN.

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Delayed Wallerian degeneration and increased neurofilament phosphorylation in sciatic nerves of rats with streptozocin-induced diabetes

Cited by 57 publications

References 29 publications

Ciliary Neurotrophic Factor Improves Nerve Conduction and Ameliorates Regeneration Deficits in Diabetic Rats

Ciliary Neurotrophic Factor Improves Nerve Conduction and Ameliorates Regeneration Deficits in Diabetic Rats

Advanced Diabetic Neuropathy: A Point of no Return?

The Beneficial Effects of C-Peptide on Diabetic Polyneuropathy

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