Oxidative stress and diabetic neuropathy: a new understanding of an old problem

Feldman, Eva L.

doi:10.1172/jci17862

Cited by 152 publications

(137 citation statements)

References 29 publications

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“…This complication is thought to arise from biochemical changes (e.g., protein glycation of cellular proteins, exaggerated flux through the polyol pathway, reduced Na ϩ ,K ϩ -ATPase, and neurotrophic factors. In addition, increased oxidative stress (26) and vascular alterations [decreased microvascular blood flow, increased vascular resistance, and altered vascular permeability (27,28)] are believed to lead to functional (decreased nerve conduction velocity and nerve blood flow) and structural abnormalities (29,30). In particular, in STZ-diabetic rats, there are evidences of apoptosis of dorsal root ganglia sensory neurons and Schwann cells (31), possibly due to oxidative stress driven by hyperglycemia (32,33).…”

Section: Discussionmentioning

confidence: 99%

“…At the biochemical level, potential etiologic mechanisms to explain the slowing of NCV during hyperglycemia include decreased activity of Na ϩ ,K ϩ -ATPase in peripheral nerves and atrophy of large myelinated fibers (30). We previously observed that the Na ϩ ,K ϩ -ATPase in the peripheral nerves is sensitive to environmental hypoxic conditions (55).…”

Section: Discussionmentioning

confidence: 99%

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Erythropoietin both protects from and reverses experimental diabetic neuropathy

Bianchi

Büyükakıllı

Brines

et al. 2004

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

238

179

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Tail-nerve conduction velocities (NCV) was assessed at 5 and 11 weeks for the preventive and therapeutic schedule, respectively. Compared to nondiabetic rats, NCV was 20% lower after 5 weeks in the STZ group, and this decrease was attenuated 50% by rhEPO. Furthermore, the reduction of Na ؉ ,K ؉ -ATPase activity of diabetic nerves (by 55%) was limited to 24% in the rhEPO-treated group. In the therapeutic schedule, NCV was reduced by 50% after 11 weeks but by only 23% in the rhEPO-treated group. rhEPO treatment attenuated the decrease in compound muscle action potential in diabetic rats. In addition, rhEPO treatment was associated with a preservation of footpad cutaneous innervation, as assessed by protein gene product 9.5 immunostaining. Diabetic rats developed alterations in mechanical and thermal nociception, which were partially reversed by rhEPO given either in a preventative or therapeutic manner. These observations suggest that administration of rhEPO or its analogues may be useful in the treatment of diabetic neuropathy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Erythropoietin both protects from and reverses experimental diabetic neuropathy

Bianchi

Büyükakıllı

Brines

et al. 2004

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

238

179

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“…In higher vertebrates, the neuron organization in the myenteric plexus forming ganglia interconnected by nerve fibers between the muscle layer strata of the gastro-intestinal segments is well described in the literature (Gabella 1979, 1990, Molinari et al 1994, Sant'Ana et al 1997, Furness 2000, Mari et al 2007, Silva et al 2008) and is not modified by diabetes (Zanoni et al 1997, 2003, Silverio et al 2008. Similarly, the plexus organization remained unchanged among the groups studied (C, CS, DS, and D), not changing either with the diabetes onset and or by the AA-supplementation.…”

Section: Discussionmentioning

confidence: 95%

“…Changes in the myenteric plexus are included in diabetic autonomic neuropathy (Araújo, 1996), whose etipatogeny has not been clarified yet (Cellek et al 2003). The polyol pathway activity, among others, can be changed due to direct or indirect the intensification of the oxidative stress mediated by the hyperglycemia (Davison et al 2002, Feldman 2003. In diabetes, the AA administration, an antioxidant substance and aldose reductase inhibitor [a fundamental enzyme to the polyol pathway] (Levine 1986, Will & Byers 1996 is used in an attempt to minimize or prevent the deleterious consequences arising from diabetes.…”

Section: Discussionmentioning

confidence: 99%

Effects of ascorbic acid supplementation in ileum myenteric neurons of streptozotocin-induced diabetic rats

et al. 2009

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295Pesq. Vet. Bras. 29(4): 295-302, abril 2009 RESUMO.-[Efeitos da suplementação do ácido ascórbico nos neurônios mientéricos do íleo de ratos diabéticos induzidos por estreptozootocina.] A exacerbação do estresse oxidativo e da via do poliol que comprometem o plexo mioentérico são alterações metabóli-cas características do diabetes. O ácido ascórbico (AA) é antioxidante e inibidor da aldose redutase, podendo atuar como neuroprotetor. Verificaram-se os efeitos da suplementação com AA sobre o número e a área do perfil do corpo celular (PC) de neurônios mioentéricos em ratos diabéticos induzidos por estreptozootocina. Formaram-se quatro grupos com cinco animais cada: normoglicêmico (C); diabético (D); diabético tratado com AA (DS); e normoglicêmico tratado com AA (CS). Três vezes por semana administrou-se 50mg de AA para cada animal (grupos DS e CS). Após 90 dias e eutanásia com tiopental, o íleo foi coletado e processado para a técnica da NADPHdiaforase. Não se observaram diferenças (P>0,05) na densidade neuronal entre os grupos. A área do PC foi menor (P<0,05) para os grupos DS e CS, com incidência maior de neurônios com área do PC superior a 200μm 2 para os grupos C e D. Concluiu-se que o AA não influenciou a densidade neuronal do íleo, mas foi neuroprotetor The exacerbation of the oxidative stress and of the polyol pathway which impair damage myenteric plexus are metabolic characteristics of diabetes. The ascorbic acid (AA) is an antioxidant and an aldose reductase inhibitor, which may act as neuroprotector. The effects of AA supplementation on the density and cellular body profile area (CP) of myenteric neurons in STZ-induced diabetes in rats were assessed. Four groups with five animals each were formed: normoglycemic (C); diabetic (D); AA-treated diabetic (DS) and AA-treated normoglycemic (CS). Dosagen of 50mg of AA were given, three times a week, for each animal (group DS and CS). Ninety days later and after euthanasia, the ileum was collected and processed for the NADPH-diaphorase technique. There were no differences (P>0.05) in the neuronal density among the groups. The CP area was lower (P<0.05) in the DS and CS groups, with a higher incidence of neurons with a CP area exceeding 200μm 2 for groups C and D. The AA had no influence on the neuronal density in the ileum but had a neuroprotective effect, preventing the increase in the CP area and allowing a higher number of neurons with a CP area with less than 200μm 2 .INDEX TERMS: Vitamin C, diabetes, intestine, myenteric plexus.

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“…Existe também a relação com anormalidades microvasculares que provocam diminuição do fluxo sangüíneo e hipóxia neural, alteração do metabolismo de ácidos graxos, estresse oxidativo e diminuição de fatores de crescimento para os neurônios e células Schwann 32,33 .…”

Section: Neuropatia Diabéticaunclassified

Aplicações clínicas da suplementação de L-carnitina

et al. 2005

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A carnitina, uma amina quaternária (3-hidroxi-4-N-trimetilamino-butirato), é sintetizada no organismo (fígado, rins e cérebro) a partir de dois aminoácidos essenciais: lisina e metionina, exigindo para sua síntese a presença de ferro, ácido ascórbico, niacina e vitamina B 6 . Tem função fundamental na geração de energia pela célula, pois age nas reações transferidoras de ácidos graxos livres do citosol para mitocôndrias, facilitando sua oxidação e geração de adenosina Trifosfato. A concentração orgânica de carnitina é resultado de processos metabólicos -como ingestão, biossíntese, transporte dentro e fora dos tecidos e excreção -que, quando alterados em função de diversas doenças, levam a um estado carencial de carnitina com prejuízos relacionados ao metabolismo de lipídeos. A suplementação de L-carnitina pode aumentar o fluxo sangüíneo aos músculos devido também ao seu efeito vasodilatador e antioxidante, reduzindo algumas complicações de doenças isquêmicas, como a doença arterial coronariana, e as conseqüências da neuropatia diabética. Por esse motivo, o objetivo do presente trabalho foi descrever possíveis benefícios da suplementação de carnitina nos indivíduos com necessidades especiais e susceptíveis a carências de carnitina, como os portadores de doenças renais, neuropatia diabética, síndrome da imunodefeciência adquirida e doenças cardiovasculares. Termos de indexação:Síndrome de Imunodeficiência Adquirida, diabetes mellitus, doenças cardiovasculares, doenças renais, carnitina, terapêutica. A B S T R A C TCarnitine, a quaternary amine (3-hidroxy-4-n-trimethylaminobutyrate

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Oxidative stress and diabetic neuropathy: a new understanding of an old problem

Cited by 152 publications

References 29 publications

Erythropoietin both protects from and reverses experimental diabetic neuropathy

Erythropoietin both protects from and reverses experimental diabetic neuropathy

Effects of ascorbic acid supplementation in ileum myenteric neurons of streptozotocin-induced diabetic rats

Aplicações clínicas da suplementação de L-carnitina

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