ArticleThe American journal of pathology2003
Non-obese diabetic mice rapidly develop dramatic sympathetic neuritic dystrophy: a new experimental model of diabetic autonomic neuropathy.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 68 citations in OpenAlex.
- Models of hyperglycaemia in diabetes mellitus and its complications.Nature reviews. Endocrinology · 2026Review
- An orally available compound suppresses glucagon hypersecretion and normalizes hyperglycemia in type 1 diabetes.JCI insight · 2024Article
- BMECs Ameliorate High Glucose-Induced Morphological Aberrations and Synaptic Dysfunction via VEGF-Mediated Modulation of Glucose Uptake in Cortical Neurons.Cellular and molecular neurobiology · 2023Article
- Contribution of animal models to diabetes research: Its history, significance, and translation to humans.Journal of diabetes investigation · 2023Review
- Neurobiological Opportunities in Diabetic Polyneuropathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Sensory neurons derived from diabetic rats exhibit deficits in functional glycolysis and ATP that are ameliorated by IGF-1.Molecular metabolism · 2021Article
- Review
- Diabetic neuropathy research: from mouse models to targets for treatment.Neural regeneration research · 2019Review
- Wound Healing Delay in the ZDSD Rat.In vivo (Athens, Greece) · 2017Article
- Mitochondrial dysfunction in diabetic neuropathy: a series of unfortunate metabolic events.Current diabetes reports · 2015Review
- Synaptic input changes to spinal cord motoneurons correlate with motor control impairments in a type 1 diabetes mellitus model.Brain and behavior · 2015Article
- Therapeutic Potential of Adipose-Derived SSEA-3-Positive Muse Cells for Treating Diabetic Skin Ulcers.Stem cells translational medicine · 2015Article
- Article
- The p75 neurotrophin receptor is required for the major loss of sympathetic nerves from islets under autoimmune attack.Diabetes · 2014Article
- Temporal dystrophic remodeling within the intrinsic cardiac nervous system of the streptozotocin-induced diabetic rat model.Acta neuropathologica communications · 2014Article
- Diabetic gastrointestinal motility disorders and the role of enteric nervous system: current status and future directions.Neurogastroenterology and motility · 2014Review
- Animal models of diabetic neuropathy: progress since 1960s.Journal of diabetes research · 2013Review
- Cationic nanomicelles for delivery of plasmids encoding interleukin-4 and interleukin-10 for prevention of autoimmune diabetes in mice.Pharmaceutical research · 2012Article
- Altered calcium signaling in colonic smooth muscle of type 1 diabetic mice.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Effect of insulin and an erythropoietin-derived peptide (ARA290) on established neuritic dystrophy and neuronopathy in Akita (Ins2 Akita) diabetic mouse sympathetic ganglia.Experimental neurology · 2011Article
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7 authors at 1 institution in 1 country.
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Abstract
To address the pathogenesis of diabetic autonomic neuropathy, we have examined the sympathetic nervous system in non-obese diabetic (NOD) and streptozotocin (STZ)-induced diabetic mice, two models of type 1 diabetes, and the db/db mouse, a model of type 2 diabetes. After only 3 to 5 weeks of diabetes, NOD mice developed markedly swollen axons and dendrites ("neuritic dystrophy") in the prevertebral superior mesenteric and celiac ganglia (SMG-CG), similar to the pathology described in diabetic STZ- and BBW-rat and man. Comparable changes failed to develop in the superior cervical ganglia of the NOD mouse or in the SMG-CG of non-diabetic NOD siblings. STZ-induced diabetic mice develop identical changes, although at a much slower pace and to a lesser degree than NOD mice. NOD-SCID mice, which are genetically identical to NOD mice except for the absence of T and B cells, do not develop diabetes or neuropathology comparable to diabetic NOD mice. However, STZ-treated NOD-SCID mice develop severe neuritic dystrophy, evidence against an exclusively autoimmune pathogenesis for autonomic neuropathy in this model. Chronically diabetic type 2 db/db mice fail to develop neuritic dystrophy, suggesting that hyperglycemia alone may not be the critical and sufficient element. The NOD mouse appears to be a valuable model of diabetic sympathetic autonomic neuropathy with unambiguous, rapidly developing neuropathology which corresponds closely to the characteristic pathology of other rodent models and man.
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