Mitochondrial dysfunction in diabetic neuropathy: a series of unfortunate metabolic events.

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.

journal_name

Curr Diab Rep

journal_title

Current diabetes reports

authors

Fernyhough P

doi

10.1007/s11892-015-0671-9

subject

Has Abstract

pub_date

2015-11-01 00:00:00

pages

89

issue

11

eissn

1534-4827

issn

1539-0829

pii

10.1007/s11892-015-0671-9

journal_volume

15

pub_type

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