Behavioural, morphological and electrophysiological assessment of the effects of type 2 diabetes mellitus on large and small nerve fibres in Zucker diabetic fatty, Zucker lean and Wistar rats

García‐Pérez, Elizabeth; Schönberger, Tanja; Sumalla, Mireia; Stierstorfer, Birgit; Solà, Romà; Doods, Henri; Serra, Jordi; Gorodetskaya, Natalia

doi:10.1002/ejp.1235

Cited by 17 publications

(7 citation statements)

References 66 publications

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“…However, while previous studies in diabetic mice showed that heat hypoalgesia was accompanied by loss of plantar IENF and that NSI-189 restored both heat sensation and IENF density, the ZDF rats showed only a mild reduction in paw IENF density. A similar mild trend to decrease of paw IENF has been reported in ZDF rats [30], whereas others reported more marked deficits [26,31]. Survival and/or accelerated regrowth of IENF may reflect increased circulating insulin levels in the early stage, despite decreasing levels in the later stage, as sensory neuron energy balance, neurite outgrowth, and paw IENF density are modulated by insulin, independent of hyperglycemia [32][33][34][35].…”

Section: Discussionsupporting

confidence: 63%

Enhancement of Mitochondrial Function by the Neurogenic Molecule NSI-189 Accompanies Reversal of Peripheral Neuropathy and Memory Impairment in a Rat Model of Type 2 Diabetes

Jolivalt

Aghanoori

Navarro-Diaz

et al. 2022

Journal of Diabetes Research

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Aims. Mitochondrial dysfunction contributes to many forms of peripheral and central nervous system degeneration. Therapies that protect mitochondrial number and function have the potential to impact the progression of conditions such as diabetic neuropathy. We therefore assessed indices of mitochondrial function in dorsal root ganglia (DRG) and brain cortex of the Zucker diabetic fatty (ZDF) rat model of type 2 diabetes and tested the therapeutic impact of a neurogenic compound, NSI-189, on both mitochondrial function and indices of peripheral and central neurological dysfunction. Materials and Methods. ZDF rats were maintained for 16 weeks of untreated diabetes before the start of oral treatment with NSI-189 for an additional 16 weeks. Nerve conduction velocity, sensitivity to tactile and thermal stimuli, and behavioral assays of cognitive function were assessed monthly. AMP-activated protein kinase (AMPK) phosphorylation, mitochondrial protein levels, and respiratory complex activities were assessed in the DRG and brain cortex after 16 weeks of treatment with NSI-189. Results. Treatment with NSI-189 selectively elevated the expression of protein subunits of complexes III and V and activities of respiratory complexes I and IV in the brain cortex, and this was accompanied by amelioration of impaired memory function and plasticity. In the sensory ganglia of ZDF rats, loss of AMPK activity was ameliorated by NSI-189, and this was accompanied by reversal of multiple indices of peripheral neuropathy. Conclusions. Efficacy of NSI-189 against dysfunction of the CNS and PNS function in type 2 diabetic rats was accompanied by improvement of mitochondrial function. NSI-189 exhibited actions at different levels of mitochondrial regulation in central and peripheral tissues.

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Section: Discussionsupporting

confidence: 63%

Enhancement of Mitochondrial Function by the Neurogenic Molecule NSI-189 Accompanies Reversal of Peripheral Neuropathy and Memory Impairment in a Rat Model of Type 2 Diabetes

Jolivalt

Aghanoori

Navarro-Diaz

et al. 2022

Journal of Diabetes Research

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“…At present, the most objective, sensitive and reliable method to diagnose DNP is NET. NET electrophysiological examination is the gold standard for diagnosis, but the operation is complicated and costly (15)(16)(17)(18)(19), and if it is used as a routine examination item, patient compliance is poor. The screen efficiency of MNSI for DPN is better than that of the TCSS and the MNSI has the same diagnostic consistency with NET.…”

Section: Discussionmentioning

confidence: 99%

Retrospective study of the ultrasound characteristics of the tibial nerve in patients with type 2 diabetic peripheral neuropathy

et al. 2021

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Background: Ultrasound is a promising imaging examination for type 2 diabetic peripheral neuropathy (DPN). This study aimed to explore the risk factors of ultrasound diagnostic characteristics in the tibial nerves of patients with type 2 DPN. Methods:The Michigan Neuropathy Screening Instrument (MNSI) was used for neuropathy evaluation, and 520 patients with type 2 diabetes were divided into a DPN group and non-DPN (NDPN) group with 2 points as the cut-off value. The two groups were matched at a ratio of 1:1 according to age, BMI, calf circumference, and gender, resulting in 44 matched pairs. The dependent variable was type 2 DPN and the concomitant variables were the width, thickness, cross-sectional area, and unclear honeycomb-like structure of the tibial nerve. A 1:1 matched conditional logistic regression model was established to analyze which ultrasound diagnostic characteristics of the tibial nerve were risk factors for type 2 DPN.Results: The thickness (OR =5.176, P=0.043) and cross-sectional area (OR =1.659, P=0.030) of the tibial nerve were risk factors for the diagnosis of DPN, while the width and unclear honeycomb-like structure of the nerve were not (P>0.05). In the diagnosis of DPN, the area under the receiver operating characteristic (ROC) curve of the cross-sectional area of the tibial nerve was 0.747, and the sensitivity, specificity, positive predictive value, and negative predictive value were 61.36%, 95.45%, 93.10%, and 71.20%, respectively.The area under the ROC curve of tibial nerve thickness was 0.867, and the sensitivity, specificity, positive predictive value, and negative predictive value were 81.82%, 90.91%, 90.00%, and 83.30%, respectively.The area under the ROC curve of thickness was larger than that of cross-sectional area of the tibial nerve (z statistic =1.800, P=0.07). Conclusions:The thickness and cross-sectional area of the tibial nerve measured by ultrasound are risk factors for type 2 DPN. The diagnostic sensitivity of the thickness is higher than the cross-sectional area, while the diagnostic specificity of the cross-sectional area is higher than the thickness.

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“…Axonal degeneration, with both primary and secondary demyelination, has been documented in nerve biopsies from both animal models and individuals with diabetic polyneuropathy [ 20 , 21 ]. In particular, impairment of the myelin sheath and Schwann cells has been shown.…”

Section: Pathophysiology Of Peripheral Neuropathy In Diabetesmentioning

confidence: 99%

Peripheral Neuropathy in Diabetes Mellitus: Pathogenetic Mechanisms and Diagnostic Options

Galiero

Caturano

Vetrano

et al. 2023

IJMS

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Diabetic neuropathy (DN) is one of the main microvascular complications of both type 1 and type 2 diabetes mellitus. Sometimes, this could already be present at the time of diagnosis for type 2 diabetes mellitus (T2DM), while it appears in subjects with type 1 diabetes mellitus (T1DM) almost 10 years after the onset of the disease. The impairment can involve both somatic fibers of the peripheral nervous system, with sensory-motor manifestations, as well as the autonomic system, with neurovegetative multiorgan manifestations through an impairment of sympathetic/parasympathetic conduction. It seems that, both indirectly and directly, the hyperglycemic state and oxygen delivery reduction through the vasa nervorum can determine inflammatory damage, which in turn is responsible for the alteration of the activity of the nerves. The symptoms and signs are therefore various, although symmetrical painful somatic neuropathy at the level of the lower limbs seems the most frequent manifestation. The pathophysiological aspects underlying the onset and progression of DN are not entirely clear. The purpose of this review is to shed light on the most recent discoveries in the pathophysiological and diagnostic fields concerning this complex and frequent complication of diabetes mellitus.

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Behavioural, morphological and electrophysiological assessment of the effects of type 2 diabetes mellitus on large and small nerve fibres in Zucker diabetic fatty, Zucker lean and Wistar rats

Cited by 17 publications

References 66 publications

Enhancement of Mitochondrial Function by the Neurogenic Molecule NSI-189 Accompanies Reversal of Peripheral Neuropathy and Memory Impairment in a Rat Model of Type 2 Diabetes

Enhancement of Mitochondrial Function by the Neurogenic Molecule NSI-189 Accompanies Reversal of Peripheral Neuropathy and Memory Impairment in a Rat Model of Type 2 Diabetes

Retrospective study of the ultrasound characteristics of the tibial nerve in patients with type 2 diabetic peripheral neuropathy

Peripheral Neuropathy in Diabetes Mellitus: Pathogenetic Mechanisms and Diagnostic Options

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