Neuroskeletal Effects of Chronic Bioelectric Nerve Stimulation in Health and Diabetes
| Autor: | Alec T Beeve, Erica L. Scheller, Xiao Zhang, Ying Yan, Matthew R. MacEwan, Ivana Shen, Kristann L. Magee |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
medicine.medical_specialty
Bone disease muscle Context (language use) type 1 diabetes (T1D) gait bone bone marrow adiposity lcsh:RC321-571 Diabetes mellitus Internal medicine medicine electrical stimulation lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry Original Research nerves business.industry General Neuroscience medicine.disease Neuromodulation (medicine) medicine.anatomical_structure Peripheral neuropathy Sarcopenia Cardiology Cortical bone neuropathy Sciatic nerve business Cancellous bone Neuroscience |
| Zdroj: | Frontiers in Neuroscience, Vol 15 (2021) Frontiers in Neuroscience |
| ISSN: | 1662-4548 |
| Popis: | Background/AimsBioelectric nerve stimulation (eStim) is a novel clinical paradigm that can promote nerve regeneration after trauma, including within the context of diabetes. However, its ability to prevent the onset of diabetic peripheral neuropathy (DPN) has not yet been evaluated. Beyond the nerve itself, DPN has emerged as a potential contributor to sarcopenia and bone disease; thus, we hypothesized that eStim could serve as a strategy to simultaneously promote neural and musculoskeletal health in diabetes.MethodsTo address this question, an eStim paradigm pre-optimized to promote nerve regeneration was applied to the sciatic nerve, which directly innervates the tibia and lower limb, for 8-weeks in control and streptozotocin-induced type 1 diabetic (T1D) rats. Metabolic, gait, nerve and bone assessments were used to evaluate the progression of diabetes and the effect of sciatic nerve eStim on neuropathy and musculoskeletal disease, while also considering the effects of cuff placement and chronic eStim in otherwise healthy animals.ResultsRats with T1D exhibited increased mechanical allodynia in the hindpaw, reduced muscle mass, decreased cortical and cancellous bone volume fraction (BVF), reduced cortical bone tissue mineral density (TMD), and decreased bone marrow adiposity. T1D also had an independent effect on gait. Placement of the cuff electrode alone was sufficient to alter gait patterns and to promote unilateral reductions in tibia length, cortical BVF, and bone marrow adiposity. Alterations in gait patterns and left-right balance to tibia length were restored with eStim, but it did not prevent T1D-induced changes in muscle, bone, marrow adiposity or mechanical sensitivity. Beyond this, chronic eStim resulted in an independent, bilateral reduction in cortical TMD.ConclusionOverall, these results provide new insight into the pathogenesis of diabetic neuroskeletal disease and its regulation by eStim. Though eStim did not prevent neural or musculoskeletal complications in T1D, our results demonstrate that clinical applications of peripheral neuromodulation ought to consider the impact of device placement and eStim on long-term skeletal health in both healthy individuals and those with metabolic disease. This includes monitoring for compounded bone loss to prevent unintended consequences including decreased bone mineral density and increased fracture risk. |
| Databáze: | OpenAIRE |
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