ArticleDiabetologia2004
Evaluation of orally active poly(ADP-ribose) polymerase inhibitor in streptozotocin-diabetic rat model of early peripheral neuropathy.
Article in Diabetologia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 79 citations in OpenAlex.
- Role of Exogenous Pyruvate in Maintaining Adenosine Triphosphate Production under High-Glucose Conditions through PARP-Dependent Glycolysis and PARP-Independent Tricarboxylic Acid Cycle.International journal of molecular sciences · 2024Article
- Diabetic Neuropathy: An Overview of Molecular Pathways and Protective Mechanisms of Phytobioactives.Endocrine, metabolic & immune disorders drug targets · 2024Review
- NADInternational journal of molecular sciences · 2022Article
- Prospects for the application of transcranial magnetic stimulation in diabetic neuropathy.Neural regeneration research · 2021Review
- The Effects of Exercise on Cerebellar Growth-Associated Protein 43 and Adenylyl Cyclase- Associated Protein 1 Gene Expression and Proteins in Diabetic-Induced Neuropathy and Healthy Male Wistar Rats.International journal of preventive medicine · 2021Article
- A streptozotocin-induced diabetic neuropathic pain model for static or dynamic mechanical allodynia and vulvodynia: validation using topical and systemic gabapentin.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Mitochondrial dysfunction in diabetic neuropathy: a series of unfortunate metabolic events.Current diabetes reports · 2015Review
- Protective Pleiotropic Effect of Flavonoids on NAD⁺ Levels in Endothelial Cells Exposed to High Glucose.Oxidative medicine and cellular longevity · 2015Article
- Mouse models of diabetic neuropathy.ILAR journal · 2014Review
- Therapeutic applications of PARP inhibitors: anticancer therapy and beyond.Molecular aspects of medicine · 2013Review
- Accelerated aging during chronic oxidative stress: a role for PARP-1.Oxidative medicine and cellular longevity · 2013Article
- Insulin in central nervous system: more than just a peripheral hormone.Journal of aging research · 2012Article
- Nutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetes.Mitochondrion · 2011Review
- PARP inhibition alleviates diabetes-induced systemic oxidative stress and neural tissue 4-hydroxynonenal adduct accumulation: correlation with peripheral nerve function.Free radical biology & medicine · 2011Article
- Animal models and biomarkers of neuropathy in diabetic rodents.Indian journal of pharmacology · 2010Article
- New therapeutic and biomarker discovery for peripheral diabetic neuropathy: PARP inhibitor, nitrotyrosine, and tumor necrosis factor-{alpha}.Endocrinology · 2010Article
- Article
- Diabetic painful and insensate neuropathy: pathogenesis and potential treatments.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009Review
- Peripheral neuropathy in mice with neuronal nitric oxide synthase gene deficiency.International journal of molecular medicine · 2009Article
- Role of nitrosative stress in the pathogenesis of diabetic vascular dysfunction.British journal of pharmacology · 2009Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
aims/hypothesisPoly(ADP-ribose) polymerase activation depletes NAD+ and high-energy phosphates, activates protein kinase C, and affects gene expression in various tissues. This study was designed to characterise the effects of the potent, orally active poly(ADP-ribose) polymerase inhibitor PJ34 in the Wistar rat model of early diabetic neuropathy.
methodsControl and streptozotocin-diabetic rats were maintained with or without PJ34 treatment (30 mg x kg(-1) x day(-1)) for two weeks, after two weeks without treatment. Endoneurial blood flow was assessed by hydrogen clearance; metabolites and high-energy phosphates were assayed by enzymatic spectrofluorometric methods; and poly(ADP-ribose) was detected by immunohistochemistry.
resultsBlood glucose concentrations were increased to a similar extent in untreated and PJ34-treated diabetic rats compared with controls. Intense poly(ADP-ribose) immunostaining was observed in the sciatic nerve of diabetic rats, but not in other groups. Final sciatic motor nerve conduction velocity and digital sensory nerve conduction velocity were reduced by 24% and 22% respectively in diabetic rats compared with controls (p<0.01 for both), and both were 98% corrected by PJ34 (p<0.01 vs diabetic group for both). In contrast, with PJ34 treatment, nerve blood flow showed a modest (17%) increase, and vascular conductance showed a tendency to increase. Free mitochondrial and cytosolic NAD+:NADH ratios, assessed from the glutamate and lactate dehydrogenase systems, phosphocreatine concentrations, and phosphocreatine:creatine ratios were decreased in diabetic rats and essentially normalised by PJ34. In both untreated and PJ34-treated diabetic rats, nerve glucose, sorbitol and fructose were increased to a similar extent. PJ34 did not affect any variables in control rats. CONCLUSIONS/
interpretationShort-term poly(ADP-ribose) polymerase inhibitor treatment reverses functional and metabolic abnormalities of early diabetic neuropathy. Complete normalisation of nerve blood flow is not required for correction of motor or sensory nerve conduction velocities, provided that a therapeutic agent can restore nerve energy state via direct action on Schwann cells.
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