Therapeutic Strategies for Diabetic Neuropathy

Habib, Ali A; Brannagan, Thomas H.

doi:10.1007/s11910-010-0093-7

Cited by 38 publications

(23 citation statements)

References 54 publications

(51 reference statements)

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“…The observed increase in small myelinated fibre profiles in sciatic nerve trunk may represent large fibre neuropathy, with demyelination of larger fibres [25], and hence smaller apparent cross sectional area both in the nerve fibre and somata. Myelin damage could affect sensory fibres or motor axons, although hyperglycaemia has been shown to affect sensory fibres to a greater extent than motor axons [35]. Activated caspase-3 coexpression with NF200 in DRG neurons is also consistent with this interpretation.…”

Section: Discussionmentioning

confidence: 59%

Vascular endothelial growth factor-A165b prevents diabetic neuropathic pain and sensory neuronal degeneration

et al. 2015

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Section: Discussionmentioning

confidence: 59%

Vascular endothelial growth factor-A165b prevents diabetic neuropathic pain and sensory neuronal degeneration

et al. 2015

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“…He goes on to describe that the Kumomoto study (Shichiri 2000) revealed a similar effect in people with type 2 diabetes, which was later supported by the UKPDSStudy Group 1998. In 2010, Habib 2010 and Stolar 2010 both emphasized the DCCT findings. Stolar 2010 go on to describe the UKPDS Study Group 1998 as well.…”

Section: Discussionmentioning

confidence: 99%

Enhanced glucose control for preventing and treating diabetic neuropathy

Callaghan

Little

Feldman

et al. 2012

Cochrane Database of Systematic Reviews

396

334

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Background There are two types of diabetes. Type 1 diabetes affects younger people and needs treatment with insulin injections. Type 2 diabetes affects older people and can usually be treated by diet and oral drugs. Diabetic neuropathy affects 10% of patients with diabetes mellitus at diagnosis and 40% to 50% after 10 years. Enhanced glucose control is the best studied intervention for the prevention of this disabling condition but there have been no systematic reviews of the evidence. Objectives To examine the evidence for enhanced glucose control in the prevention of distal symmetric polyneuropathy in people with type 1 and type 2 diabetes. Search methods We searched the Cochrane Neuromuscular Disease Group Specialized Register (30 January 2012), CENTRAL (2012, Issue 1), MED-LINE (1966 to January 2012) and EMBASE (1980 to January 2012) for randomized controlled trials of enhanced glucose control in diabetes mellitus. Selection criteria We included all randomized, controlled studies investigating enhanced glycemic control that reported neuropathy outcomes after at least one year of intervention. Our primary outcome measure was annual development of clinical neuropathy defined by a clinical scale. Secondary outcomes included motor nerve conduction velocity and quantitative vibration testing. Data collection and analysis Two authors independently reviewed all titles and abstracts identified by the database searches for inclusion. Two authors abstracted data from all included studies with a standardized form. A third author mediated conflicts. We analyzed the presence of clinical neuropathy with annualized risk differences (RDs), and conduction velocity and quantitative velocity measurements with mean differences per year. Main results This review identified 17 randomized studies that addressed whether enhanced glucose control prevents the development of neuropathy. Seven of these studies were conducted in people with type 1 diabetes, eight in type 2 diabetes, and two in both types. A meta-analysis of the two studies that reported the primary outcome (incidence of clinical neuropathy) with a total of 1228 participants with type 1 diabetes revealed a significantly reduced risk of developing clinical neuropathy in those with enhanced glucose control, an annualized RD of −1.84% (95% confidence interval (CI) −1.11 to −2.56). In a similar analysis of four studies that reported the primary outcome, involving 6669 participants with type 2 diabetes, the annualized RD of developing clinical neuropathy was −0.58% (95% CI 0.01 to −1.17). Most secondary outcomes were significantly in favor of intensive treatment in both populations. However, both types of diabetic participants also had a significant increase in severe adverse events including hypoglycemic events. Authors’ conclusions According to high-quality evidence, enhanced glucose control significantly prevents the development of clinical neuropathy and reduces nerve conduction and vibration threshold abnormalities in type 1 diabetes mellitus. In type 2 diab...

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“…Intensive metabolic control of blood glucose reduces the incidence of new clinically detected neuropathy, but diabetes patients can still develop DPN (78). Intensified glucose-lowering therapy increases the risk of hypoglycemic episodes and can even be dangerous (79,80).…”

Section: Activation Of Plcβ3 Causes An Increase In Intracellular Camentioning

confidence: 99%

Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db ⁻ /db ⁻ mouse, a type 2 diabetes model

Shi

Zhang

Zeberg³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Diabetic peripheral neuropathy (DPN) is the most common complication in both type 1 and type 2 diabetes. Here we studied some phenotypic features of a well-established animal model of type 2 diabetes, the leptin receptor-deficient db − /db − mouse, and also the effect of long-term (6 mo) treatment with coenzyme Q10 (CoQ10), an endogenous antioxidant. Diabetic mice at 8 mo of age exhibited loss of sensation, hypoalgesia (an increase in mechanical threshold), and decreases in mechanical hyperalgesia, cold allodynia, and sciatic nerve conduction velocity. All these changes were virtually completely absent after the 6-mo, daily CoQ10 treatment in db − /db − mice when started at 7 wk of age. There was a 33% neuronal loss in the lumbar 5 dorsal root ganglia (DRGs) of the db − /db − mouse versus controls at 8 mo of age, which was significantly attenuated by CoQ10. There was no difference in neuron number in 5/6-wk-old mice between diabetic and control mice. We observed a strong down-regulation of phospholipase C (PLC) β3 in the DRGs of diabetic mice at 8 mo of age, a key molecule in pain signaling, and this effect was also blocked by the 6-mo CoQ10 treatment. Many of the phenotypic, neurochemical regulations encountered in lumbar DRGs in standard models of peripheral nerve injury were not observed in diabetic mice at 8 mo of age. These results suggest that reactive oxygen species and reduced PLCβ3 expression may contribute to the sensory deficits in the late-stage diabetic db − /db − mouse, and that early long-term administration of the antioxidant CoQ10 may represent a promising therapeutic strategy for type 2 diabetes neuropathy.is a debilitating complication of both type 1 and type 2 diabetes, affecting up to 50% of diabetes patients (1-5). DPN can be observed early in human diabetes (6, 7). Early neurophysiological studies indicated that at initial stages of the illness, the severity of the polyneuropathy was similar in type 1 and type 2 diabetes patients (8). However, more recent studies showed distinct differences both in humans and rodent models. Thus, progressive axonal atrophy and loss are more serious in type 1 diabetes, which in contrast to type 2 shows nodal and paranodal degenerative changes, as well as more severe downstream effects on neuroskeletal and adhesive proteins (9).In type 1 and type 2 diabetes, many patients initially experience painful diabetic neuropathy, allodynia, which subsides and then is replaced by loss of sensation, hypoalgesia (5, 10, 11). A similar course of disease has been noted in the db /db− mouse, just one of many animal models of diabetes (SI Text), has since then been extensively studied as a particularly robust model for type 2 DPN (14).Previous studies of mammalian DPN models have reported a decrease in impulse conduction velocity (CV) in several peripheral nerves, interpreted as being caused by a reduction in number of large or medium-sized axons (15-20), demyelination (18,19,(21)(22)(23), or axon shrinkage/atrophy (24, 25). Unmyelinated and myelinated fibers in the skin a...

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Therapeutic Strategies for Diabetic Neuropathy

Cited by 38 publications

References 54 publications

Vascular endothelial growth factor-A165b prevents diabetic neuropathic pain and sensory neuronal degeneration

Vascular endothelial growth factor-A165b prevents diabetic neuropathic pain and sensory neuronal degeneration

Enhanced glucose control for preventing and treating diabetic neuropathy

Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db ⁻ /db ⁻ mouse, a type 2 diabetes model

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Therapeutic Strategies for Diabetic Neuropathy

Cited by 38 publications

References 54 publications

Vascular endothelial growth factor-A165b prevents diabetic neuropathic pain and sensory neuronal degeneration

Vascular endothelial growth factor-A165b prevents diabetic neuropathic pain and sensory neuronal degeneration

Enhanced glucose control for preventing and treating diabetic neuropathy

Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db − /db − mouse, a type 2 diabetes model

Contact Info

Product

Resources

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Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db ⁻ /db ⁻ mouse, a type 2 diabetes model