Zinc Supplementation Alleviates Diabetic Peripheral Neuropathy by Inhibiting Oxidative Stress and Upregulating Metallothionein in Peripheral Nerves of Diabetic Rats

2014 ◽  
Vol 158 (2) ◽  
pp. 211-218 ◽  
Author(s):  
Fangyao liu ◽  
Feiyu Ma ◽  
Gengbin Kong ◽  
Kezhou Wu ◽  
Zhihua Deng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Peripheral Nerves ◽  
Zinc Supplementation ◽  
Diabetic Rats

scholarly journals Diabetic peripheral neuropathy: epidemiology, pathogenesis, clinic, diagnostics, treatment

2016 ◽  
Vol 24 (4) ◽  
pp. 139-151 ◽  
Author(s):  
A N Belova ◽  
M N Kudykin ◽  
G E Sheiko
Keyword(s):  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Peripheral Nerves ◽  
Pain Syndrome ◽  
Common Complication ◽  
Review Of Literature ◽  
Chronic Hyperglycemia ◽  
Progressive Degeneration ◽  
Pathophysiologic Mechanisms

The article contains the review of literature data dedicated to the most common complication associated with diabetes mellitus (DM) - the diabetic peripheral neuropathy (DPN). DPN is regarded as economic burden for any state and significantly influences the quality of patient’s life. DPN is characterized by progressive degeneration of peripheral nerves that leads to pain syndrome, movement disorders and loss of sensation. There is a set of theories of development of DPN, but the major etiological factor is the chronic hyperglycemia. The article describes pathophysiologic mechanisms of DPN development. It is noted that considering high variability of clinical pattern DPN has no unified classification. The article addresses issues related to diagnostics and criteria of establishing the diagnosis. Special attention of the article is dedicated to pathogenic and expected treatment methods.

scholarly journals Long Non-coding RNA XIST Attenuates Diabetic Peripheral Neuropathy by Inducing Autophagy Through MicroRNA-30d-5p/sirtuin1 Axis

2021 ◽  
Vol 8 ◽  
Author(s):  
Bei-Yan Liu ◽  
Lin Li ◽  
Li-Wei Bai ◽  
Chang-Shui Xu
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Schwann Cells ◽  
Diabetic Peripheral Neuropathy ◽  
Beclin 1 ◽  
Diabetic Mice ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Diabetic peripheral neuropathy (DPN) is a prevalent diabetes mellitus (Feldman et al., 2017) complication and the primary reason for amputation. Meanwhile, long non-coding RNAs (lncRNAs) are a type of regulatory non-coding RNAs (ncRNAs) that broadly participate in DPN development. However, the correlation of lncRNA X-inactive specific transcript (XIST) with DPN remains unclear. In this study, we were interested in the role of XIST in the modulation of DPN progression. Significantly, our data showed that the expression of XIST and sirtuin1 (SIRT1) was inhibited, and the expression of microRNA-30d-5p (miR-30d-5p) was enhanced in the trigeminal sensory neurons of the diabetic mice compared with the normal mice. The levels of LC3II and Beclin-1 were inhibited in the diabetic mice. The treatment of high glucose (HG) reduced the XIST expression in Schwann cells. The apoptosis of Schwann cells was enhanced in the HG-treated cells, but the overexpression of XIST could block the effect in the cells. Moreover, the levels of LC3II and Beclin-1 were reduced in the HG-treated Schwann cells, while the overexpression of XIST was able to reverse this effect. The HG treatment promoted the production of oxidative stress, while the XIST overexpression could attenuate this result in the Schwann cells. Mechanically, XIST was able to sponge miR-30d-5p and miR-30d-5p-targeted SIRT1 in the Schwann cells. MiR-30d-5p inhibited autophagy and promoted oxidative stress in the HG-treated Schwann cells, and SIRT1 presented a reversed effect. MiR-30d-5p mimic or SIRT1 depletion could reverse XIST overexpression-mediated apoptosis and autophagy of the Schwann cells. Thus, we concluded that XIST attenuated DPN by inducing autophagy through miR-30d-5p/SIRT1 axis. XIST and miR-30d-5p may be applied as the potential targets for DPN therapy.

scholarly journals TSH Combined with TSHR Aggravates Diabetic Peripheral Neuropathy by Promoting Oxidative Stress and Apoptosis in Schwann Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-23
Author(s):  
Jingwen Fan ◽  
Qi Pan ◽  
Qun Gao ◽  
Wenqing Li ◽  
Fei Xiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Cell Model ◽  
Cell Damage ◽  
Motor Nerve ◽  
Thyroid Stimulating Hormone ◽  
Motor Nerve Conduction Velocity ◽  
The Impact

Subclinical hypothyroidism (SCH) is associated with diabetic peripheral neuropathy (DPN); however, the mechanism underlying this association remains unknown. This study is aimed at examining neurofunctional and histopathological alterations in a type 2 diabetes (T2DM) mouse model of SCH and investigating the impact of thyroid-stimulating hormone (TSH) in an in vitro DPN cell model established using RSC96 cells under high glucose (HG) and palmitic acid (PA) stimulation. Our results indicated that T2DM, in combination with SCH, aggravated abnormal glucose and lipid metabolism in T2DM and dramatically destroyed the peripheral nervous system by increasing paw withdrawal latency, decreasing motor nerve conduction velocity, and exacerbating ultrastructural deterioration of the damaged sciatic nerve caused by diabetes. Furthermore, the results of our in vitro experiments showed that TSH intensified HG/PA-induced RSC96 cell damage by inducing oxidative stress, mitochondrial dysfunction, and apoptosis. More importantly, TSHR knockout or inhibition of PA-induced TSHR palmitoylation could alleviate the apoptosis induced by TSH. Overall, in this study, the novel mechanisms by which TSH, as an independent risk factor for DPN progression, aggravating Schwann cell apoptosis and demyelination, are elucidated. These findings indicate that TSHR could be a potential target for both the prevention and treatment of DPN and, possibly, other microvascular diseases, and have implication in the clinical management of patients with DPN.

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