Reduced sensory and motor conduction velocity in 25-week-old diabetic [] mice

Moore, Steven A.; Peterson, Richard G.; Felten, David L.; T, Cartwright; O’Connor, Brian L.

doi:10.1016/0014-4886(80)90181-8

Cited by 41 publications

(17 citation statements)

References 9 publications

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“…In summary, behavioral, electrophysiological and anatomical assessments of DN are profoundly impaired in the BKS-db/db mice. Our published data [13] agree with previous reports of DN in this model [33,34,[81][82][83][84][85].…”

Section: An Example Of Murine Phenotypingsupporting

confidence: 92%

“…Percent decreases in sensory nerve conduction velocities vary from 10% in the Swiss Wistar mouse following 36 weeks of diabetes to 53% in the BKS-db/db mouse 4 weeks after the onset of diabetes [36]. In the literature and in our own laboratory, the BKS-db/db mouse model of type 2 diabetes exhibits the most robust changes in both motor and sensory nerve conduction velocities with no less than a 20% decrease in either measure [13,34,36]. In models of type 1 diabetes, both inbred and outbred strains, induced or spontaneous, larger decreases are noted in motor (~24%) than sensory (~20%) conduction velocities.…”

Section: Guidelines For Disease Definitionmentioning

confidence: 85%

“…The BKS-db/db mouse is an example of a spontaneous model of type 2 diabetes that develops a robust DN. Previous work in this model demonstrated clear deficits in NCV [33,34,[81][82][83][84][85] and fiber density and/or morphology [33,35,[81][82][83][86][87][88] following the development of diabetes. BKS-db/db mice develop hyperglycemia between 3-4 weeks of age (http:// jaxmice.jax.org/) and a profound neuropathy at 24 weeks post onset of diabetes [13].…”

Section: An Example Of Murine Phenotypingmentioning

confidence: 99%

“…DN is reported as early as 4 weeks post onset of diabetes as measured by an increase in thermal latency. Both sensory and motor nerve conduction velocities are decreased [13,14,[33][34][35][36], axonal transport is slowed [37,38] and both neurotransmitter levels [39] and IENF densities are decreased [13,14] (Table 1). A second spontaneous model of type 2 diabetes is the B6.V-Lep ob /J or B6-ob/ob mouse.…”

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confidence: 99%

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Criteria for Creating and Assessing Mouse Models of Diabetic Neuropathy

Sullivan

Lentz²,

Roberts

et al. 2008

CDT

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Diabetic neuropathy (DN) is a serious and debilitating complication of both type 1 and type 2 diabetes. Despite intense research efforts into multiple aspects of this complication, including both vascular and neuronal metabolic derangements, the only treatment remains maintenance of euglycemia. Basic research into the mechanisms responsible for DN relies on using the most appropriate animal model. The advent of genetic manipulation has moved mouse models of human disease to the forefront. The ability to insert or delete genes affected in human patients offers unique insight into disease processes; however, mice are still not humans and difficulties remain in interpreting data derived from these animals. A number of studies have investigated and described DN in mice but it is difficult to compare these studies with each other or with human DN due to experimental differences including background strain, type of diabetes, method of induction and duration of diabetes, animal age and gender. This review describes currently used DN animal models. We followed a standardized diabetes induction protocol and designed and implemented a set of phenotyping parameters to classify the development and severity of DN. By applying standard protocols, we hope to facilitate the comparison and characterization of DN across different background strains in the hope of discovering the most human like model in which to test potential therapies. KeywordsNOD; Akita; ob/ob; db/db; outbred mice; nerve conduction velocity; intraepidermal nerve fiber density DIABETES MELLITUSThe term "diabetes mellitus" describes a number of conditions in which blood glucose is elevated including insulin dependent diabetes mellitus (IDDM) Beyond effective control of glucose levels, there are no treatments to prevent or cure DN. Numerous factors have impeded laboratory investigations aimed at the development of effective therapies, including an incomplete analysis of existing animal models that develop DN, lack of consistency among mouse models (diabetes induction and genetics) and lack of consensus concerning phenotyping methods. The AMDCC was formed by the NIH to develop new animal models of diabetes and its complications; its goal is to identify the most appropriate animal models to study the etiology, prevention and treatment of diabetic complications. The group has reported its findings comparing the effects of diabetes on cardiovascular disease [2], and nephropathy [12] in inbred mice from different genetic background strains and maintains a website containing its recommended phenotyping protocols. AMDCC investigators continue to refine genetic and dietary factors that affect the development of diabetes and its complications, potential interactions and overlap of complications within a genetic model, and common pathways that may influence treatment paradigms in human patients.In order to provide a consistent method of examining DN in diabetic mouse models, our laboratory implemented a standardized diabetes induction protocol used by the AMDCC (...

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Section: An Example Of Murine Phenotypingsupporting

confidence: 92%

Section: Guidelines For Disease Definitionmentioning

confidence: 85%

Section: An Example Of Murine Phenotypingmentioning

confidence: 99%

mentioning

confidence: 99%

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Criteria for Creating and Assessing Mouse Models of Diabetic Neuropathy

Sullivan

Lentz²,

Roberts

et al. 2008

CDT

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“…However, conduction deficits have been measured in several sensory and motor nerve branches [28,29]. Anatomical differences, particularly a reduction in fibre size, have been seen with diabetes [28].…”

Section: Discussionmentioning

confidence: 99%

The effects of Sorbinil on peripheral nerve conduction velocity, polyol concentrations and morphology in the streptozotocin-diabetic rat

et al. 1986

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Summary. This study examined the effects of an aldose reductase inhibitor, Sorbinil, on neuropathy over a 6-month period in streptozotocin-diabetic rats. Sorbinil treatment prevented the 10-fold increase in nerve sorbitol found with diabetes. It produced a 60% improvement in tibial nerve motor conduction velocity after 6 months. Morphometric profiles of nerves were also normalised. Axon area was reduced by 14% in untreated diabetic rats compared to age-matched controls, whereas Sorbinil-treated animals showed normal age-related axon growth. Myelin area was increased by 28% in untreated diabetic animals, but was the same as age-matched controls with Sorbinil treatment. Nerve myo-inositol levels were reduced by 45% after three months of untreated diabetes, but were normal after six months. Sorbinil treatmend tended to restore myo-inositol levels toward normal over the shorter time period. It was concluded that axon growth retardation is the most likely cause of the conduction deficit seen in longterm experimental diabetes.

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Diabetic neuropathy - a continuing enigma

Sugimoto

Murakawa

Sima

2000

Diabetes Metab. Res. Rev.

163

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In this article we will review the clinical signs and symptoms of diabetic somatic polyneuropathy (DPN), its prevalence and clinical management. Staging and classification of DPN will be exemplified by various staging paradigms of varied sophistication. The results of therapeutic clinical trials will be summarized. The pathogenesis of diabetic neuropathy reviews an extremely complex issue that is still not fully understood. Various recent advances in the understanding of the disease will be discussed, particularly with respect to the differences between neuropathy in the two major types of diabetes. The neuropathology and natural history of diabetic neuropathy will be discussed pointing out the heterogeneities of the disease. Finally, the various prospective therapeutic avenues will be dealt with and discussed.

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Reduced sensory and motor conduction velocity in 25-week-old diabetic [] mice

Cited by 41 publications

References 9 publications

Criteria for Creating and Assessing Mouse Models of Diabetic Neuropathy

Criteria for Creating and Assessing Mouse Models of Diabetic Neuropathy

The effects of Sorbinil on peripheral nerve conduction velocity, polyol concentrations and morphology in the streptozotocin-diabetic rat

Diabetic neuropathy - a continuing enigma

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