The impact of bodyweight and body condition on behavioral testing for painful diabetic neuropathy in the streptozotocin rat model

Hoybergs, Yves; Biermans, R.; Meert, Theo

doi:10.1016/j.neulet.2008.02.051

Cited by 33 publications

(23 citation statements)

References 27 publications

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“…Meanwhile, blood glucose level rose immediately after the STZ injection, reached quite a high level at first week, and then remained approximately at a stable value. The results of the current study have confirmed previous findings that blood glucose level is elevated and body weight is decreased in diabetic rats after STZ administration [38], [39]. Our results also revealed that PEMF stimulation did not significantly prevent the weight loss caused by diabetes, which is consistent to a previous investigation [36].…”

Section: Discussionsupporting

confidence: 92%

Therapeutic Effects of 15 Hz Pulsed Electromagnetic Field on Diabetic Peripheral Neuropathy in Streptozotocin-Treated Rats

et al. 2013

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Although numerous clinical studies have reported that pulsed electromagnetic fields (PEMF) have a neuroprotective role in patients with diabetic peripheral neuropathy (DPN), the application of PEMF for clinic is still controversial. The present study was designed to investigate whether PEMF has therapeutic potential in relieving peripheral neuropathic symptoms in streptozotocin (STZ)-induced diabetic rats. Adult male Sprague–Dawley rats were randomly divided into three weight-matched groups (eight in each group): the non-diabetic control group (Control), diabetes mellitus with 15 Hz PEMF exposure group (DM+PEMF) which were subjected to daily 8-h PEMF exposure for 7 weeks and diabetes mellitus with sham PEMF exposure group (DM). Signs and symptoms of DPN in STZ-treated rats were investigated by using behavioral assays. Meanwhile, ultrastructural examination and immunohistochemical study for vascular endothelial growth factor (VEGF) of sciatic nerve were also performed. During a 7-week experimental observation, we found that PEMF stimulation did not alter hyperglycemia and weight loss in STZ-treated rats with DPN. However, PEMF stimulation attenuated the development of the abnormalities observed in STZ-treated rats with DPN, which were demonstrated by increased hind paw withdrawal threshold to mechanical and thermal stimuli, slighter demyelination and axon enlargement and less VEGF immunostaining of sciatic nerve compared to those of the DM group. The current study demonstrates that treatment with PEMF might prevent the development of abnormalities observed in animal models for DPN. It is suggested that PEMF might have direct corrective effects on injured nerves and would be a potentially promising non-invasive therapeutic tool for the treatment of DPN.

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Section: Discussionsupporting

confidence: 92%

Therapeutic Effects of 15 Hz Pulsed Electromagnetic Field on Diabetic Peripheral Neuropathy in Streptozotocin-Treated Rats

et al. 2013

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“…Values represent the means ± SD. condition in the medium body weight and heavier groups (19). However, in the present study, a rapid increase in body weight was observed in the control groups (C-Ex1 and C-Sed); this was associated with overeating after exercise training.…”

Section: Discussioncontrasting

confidence: 68%

Muscle NT-3 levels increased by exercise training contribute to the improvement in caudal nerve conduction velocity in diabetic rats

Zhang

et al. 2012

Mol Med Report

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Abstract. The aim of the present study was to explore the role of exercise in diabetic peripheral neuropathy (DPN) and the mechanisms involved. For this purpose, 31 male SpragueDawley rats were used. The rats were assigned to 5 groups: diabetic rats subjected to exercise training (swimming) for 8 weeks (D-Ex1 group), diabetic rats subjected to exercise training for 4 weeks after 4 weeks of being sedentary (D-Ex2 group), diabetic rats which remained sedentary for 8 weeks (D-Sed group), control rats subjected to exercise training for 8 weeks (C-Ex1 group) and control rats which remained sedentary for 8 weeks (C-Sed group). Blood glucose levels and caudal nerve conduction velocity (NCV) were evaluated at 0 (baseline), 28 (4 weeks) and 56 days (8 weeks) after the induction of diabetes. The levels of neurotrophin-3 (NT-3) in skeletal muscle were measured by ELISA at the end of the experiment. Blood glucose levels in the D-Ex1 group rats decreased significantly after 8 weeks of exercise. The caudal NCV markedly decreased in all diabetic rats and significantly increased after 4 or 8 weeks of exercise training. Muscle NT-3 levels were significantly lower in the D-Sed compared to the 4 other groups. Muscle NT-3 levels positively correlated with caudal NCV. In conclusion, swimming training has a beneficial effect on DPN and muscle NT-3 levels, which could help improve caudal NCV in streptozotocin-induced diabetic rats. IntroductionDiabetic peripheral neuropathy (DPN) is one of the most common complications of diabetes and is responsible for 50-75% of non-traumatic amputations in developed countries (1,2). The streptozotocin (STZ) model is widely used to investigate experimental DPN (3). Abnormal nerve conduction is an early feature of diabetic nerve damage (4). Tesfaye et al showed that conduction velocity significantly increased after exercise in normal subjects (5). Selagzi et al found that exercise training significantly increased the compound muscle action potential amplitude and decreased motor latency in diabetic rats (4). However, little is known about the mechanisms involved in exersise improving nerve dysfunction in STZ-induced diabetic rats.Neurotrophin-3 (NT-3) is a type of neurotrophic factor that comprises a heterogeneous group of molecules produced by neurons, Schwann cells and end organs in the central and peripheral nervous system (PNS). In adults, neurotrophins of the PNS are synthesized in and released from target tissues. Skeletal muscles are such target tissues and produce neurotrophins. NT-3 plays a crucial role in mediating central nervous system plasticity and regeneration in the spinal cord and muscle. Short-term STZ-induced diabetes causes a reduction in muscle NT-3 mRNA and protein expression, which leads to a decreased retrograde axonal transport of NT-3 to the neuronal cell body and consequent sub-optimal neurotrophic support (6). Previous studies have shown that the continuous production of NT-3 by the latency-associated promoter 2 (LAP2)-driven expression of the transgene from a herpes simple...

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“…3) Given the complexity of WM configuration in the striatum and cortex, and the fact that only a limited number of animals were subjected to histology/immunohistology evaluations, no attempt was made to establish semi-quantitative correlations between the diabetes-related changes in diffusion indices and specific histopathological alterations. 4) Without glycemic control, the general conditions of the STZ-induced animals may deteriorate rapidly (Hoybergs et al, 2008). This is also the reason we performed DTI at 4 weeks after induction, but not at later time points when cognitive impairments are shown to be prominent (Idan-Feldman et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Abnormalities in the brain of streptozotocin-induced type 1 diabetic rats revealed by diffusion tensor imaging

Huang

Gao

Yang

et al. 2012

NeuroImage: Clinical

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Diabetes mellitus affects the brain. Both type 1 and type 2 diabetic patients are associated with white matter (WM) damage observable to diffusion tensor imaging (DTI). The underlying histopathological mechanisms, however, are poorly understood. The objectives of this study are 1) to determine whether streptozotocin (STZ)-induced type 1 diabetes is associated with WM damage observable to DTI; and 2) to understand the pathophysiological aspects underlying STZ-induced brain injuries. Male Sprague–Dawley rats received a single intraperitoneal injection of STZ (62 mg/kg). DTI was used to assess brain abnormalities at 4 weeks after induction, combined with histological assessments and ultrastructural analysis. Compared to controls, the STZ-induced rats showed significantly reduced fractional anisotropy (FA) in the motor/somatosensory cortex and striatum. Histologically, the cortex and striatum of the diabetic animals are characterized by demyelination and axonal degradation. In conclusion, STZ-induced diabetes is associated with striatal/cortical injuries observable to DTI. The DTI abnormalities are likely manifestations of demyelination and axonal degradation in the affected brain regions, and can potentially be used as surrogates for evaluating diabetic brain injuries.

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The impact of bodyweight and body condition on behavioral testing for painful diabetic neuropathy in the streptozotocin rat model

Cited by 33 publications

References 27 publications

Therapeutic Effects of 15 Hz Pulsed Electromagnetic Field on Diabetic Peripheral Neuropathy in Streptozotocin-Treated Rats

Therapeutic Effects of 15 Hz Pulsed Electromagnetic Field on Diabetic Peripheral Neuropathy in Streptozotocin-Treated Rats

Muscle NT-3 levels increased by exercise training contribute to the improvement in caudal nerve conduction velocity in diabetic rats

Abnormalities in the brain of streptozotocin-induced type 1 diabetic rats revealed by diffusion tensor imaging

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