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Hamid HS, Mervak CM, Münch AE, et al. Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves. Ann Clin Transl Neurol. 2014;1(10):799-812doi: 10.1002/acn3.119.
Hamid, H. S., Mervak, C. M., Münch, A. E., Robell, N. J., Hayes, J. M., Porzio, M. T., Singleton, J. R., Smith, A. G., Feldman, E. L., & Lentz, S. I. (2014). Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves. Annals of clinical and translational neurology, 1(10), 799-812. https://doi.org/10.1002/acn3.119
Hamid, Hussein S, et al. "Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves." Annals of clinical and translational neurology vol. 1,10 (2014): 799-812. doi: https://doi.org/10.1002/acn3.119
Hamid HS, Mervak CM, Münch AE, Robell NJ, Hayes JM, Porzio MT, Singleton JR, Smith AG, Feldman EL, Lentz SI. Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves. Ann Clin Transl Neurol. 2014 Oct;1(10):799-812. doi: 10.1002/acn3.119. Epub 2014 Oct 01. PMID: 25493271; PMCID: PMC4241807.
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Ann Clin Transl Neurol. 2014 Oct;1(10):799-812. doi: 10.1002/acn3.119. Epub 2014 Oct 01.

Hyperglycemia- and neuropathy-induced changes in mitochondria within sensory nerves.

Annals of clinical and translational neurology

Hussein S Hamid, Colin M Mervak, Alexandra E Münch, Nicholas J Robell, John M Hayes, Michael T Porzio, J Robinson Singleton, A Gordon Smith, Eva L Feldman, Stephen I Lentz

Affiliations

  1. University of Michigan Medical School, University of Michigan Ann Arbor, Michigan, 48109.
  2. Department of Neurology, University of Michigan Ann Arbor, Michigan, 48109.
  3. Division on Metabolism Endocrinology and Diabetes, Department of Internal Medicine, University of Michigan Ann Arbor, Michigan, 48105.
  4. Department of Neurology, University of Utah School of Medicine Salt Lake City, Utah, 84132.

PMID: 25493271 PMCID: PMC4241807 DOI: 10.1002/acn3.119

Abstract

OBJECTIVE: This study focused on altered mitochondrial dynamics as a potential mechanism for diabetic peripheral neuropathy (DPN). We employed both an in vitro sensory neuron model and an in situ analysis of human intraepidermal nerve fibers (IENFs) from cutaneous biopsies to measure alterations in the size distribution of mitochondria as a result of hyperglycemia and diabetes, respectively.

METHODS: Neurite- and nerve-specific mitochondrial signals within cultured rodent sensory neurons and human IENFs were measured by employing a three-dimensional visualization and quantification technique. Skin biopsies from distal thigh (DT) and distal leg (DL) were analyzed from three groups of patients; patients with diabetes and no DPN, patients with diabetes and confirmed DPN, and healthy controls.

RESULTS: This analysis demonstrated an increase in mitochondria distributed within the neurites of cultured sensory neurons exposed to hyperglycemic conditions. Similar changes were observed within IENFs of the DT in DPN patients compared to controls. This change was represented by a significant shift in the size frequency distribution of mitochondria toward larger mitochondria volumes within DT nerves of DPN patients. There was a length-dependent difference in mitochondria within IENFs. Distal leg IENFs from control patients had a significant shift toward larger volumes of mitochondrial signal compared to DT IENFs.

INTERPRETATION: The results of this study support the hypothesis that altered mitochondrial dynamics may contribute to DPN pathogenesis. Future studies will examine the potential mechanisms that are responsible for mitochondrial changes within IENFs and its effect on DPN pathogenesis.

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