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Erschienen in: Current Diabetes Reports 11/2015

01.11.2015 | Microvascular Complications—Neuropathy (R Pop-Busui, Section Editor)

Mitochondrial Dysfunction in Diabetic Neuropathy: a Series of Unfortunate Metabolic Events

verfasst von: Paul Fernyhough

Erschienen in: Current Diabetes Reports | Ausgabe 11/2015

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Abstract

Diabetic neuropathy is a dying back neurodegenerative disease of the peripheral nervous system where mitochondrial dysfunction has been implicated as an etiological factor. Diabetes (type 1 or type 2) invokes an elevation of intracellular glucose concentration simultaneously with impaired growth factor support by insulin, and this dual alteration triggers a maladaptation in metabolism of adult sensory neurons. The energy sensing pathway comprising the AMP-activated protein kinase (AMPK)/sirtuin (SIRT)/peroxisome proliferator-activated receptor-γ coactivator α (PGC-1α) signaling axis is the target of these damaging changes in nutrient levels, e.g., induction of nutrient stress, and loss of insulin-dependent growth factor support and instigates an aberrant metabolic phenotype characterized by a suppression of mitochondrial oxidative phosphorylation and shift to anaerobic glycolysis. There is discussion of how this loss of mitochondrial function and transition to overreliance on glycolysis contributes to the diminishment of collateral sprouting and axon regeneration in diabetic neuropathy in the context of the highly energy-consuming nerve growth cone.
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Metadaten
Titel
Mitochondrial Dysfunction in Diabetic Neuropathy: a Series of Unfortunate Metabolic Events
verfasst von
Paul Fernyhough
Publikationsdatum
01.11.2015
Verlag
Springer US
Erschienen in
Current Diabetes Reports / Ausgabe 11/2015
Print ISSN: 1534-4827
Elektronische ISSN: 1539-0829
DOI
https://doi.org/10.1007/s11892-015-0671-9

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