Cited by 82Mitochondrial Function and PathologyPain Mechanisms and TreatmentsAutophagy in Disease and Therapy

Nutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetes

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Chowdhury, Subir K. Roy, Dobrowsky, Rick T., Fernyhough, Paul·2011·Mitochondrion

Abstract

Diabetic neuropathy is a major complication of diabetes that results in the progressive deterioration of the sensory nervous system. Mitochondrial dysfunction has been proposed to play an important role in the pathogenesis of the neurodegeneration observed in diabetic neuropathy. Our recent work has shown that mitochondrial dysfunction occurs in dorsal root ganglia (DRG) sensory neurons in streptozotocin (STZ) induced diabetic rodents. In neurons, the nutrient excess associated with prolonged diabetes may trigger a switching off of AMP kinase (AMPK) and/or silent information regulator T1 (SIRT1) signaling leading to impaired peroxisome proliferator-activated receptor γ coactivator-1 (PGC-1α) expression/activity and diminished mitochondrial activity. This review briefly summarizes the alterations of mitochondrial function and proteome in sensory neurons of STZ-diabetic rodents. We also discuss the possible involvement of AMPK/SIRT/PGC-1α pathway in other diabetic models and different tissues affected by diabetes.

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Authors
Chowdhury, S. K. R., Dobrowsky, R. T., & Fernyhough, P.
Affiliations
  • University of Kansas (US)
  • St. Boniface Hospital (CA)
Venue
Mitochondrion
Publisher
Elsevier BV
Published
2011-11
Volume
11
Issue
6
Pages
845-854
ISSN
1567-7249 (ISSN-L)
OpenAlex
W2041085893
Cited by
82
References
112
Citations by year
2026: 4 · 2025: 3 · 2024: 2 · 2023: 2 · 2022: 7 · 2021: 6 · 2020: 6 · 2019: 7 · 2018: 5 · 2017: 4 · 2016: 5 · 2015: 4 · 2014: 9 · 2013: 6 · 2012: 11
FWCI
0.76
Type
journal article
Language
en
Open access
Locations
  • Mitochondrion (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • KU ScholarWorks (University of Kansas) (submittedVersion, cc-by-nc-nd)
Funders
  • CIHR (MOP-84214)
  • Juvenile Diabetes Research Foundation (1-2008-193, 1-2008-280, 17-2010-760)
  • St Boniface General Hospital and Research Foundation
  • National Institutes of Health (NS054847, DK073594)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
diabetic neuropathy, mitochondrial dysfunction, mitochondrial proteome, sensory neurons, dorsal root ganglia, nutrient excess, AMPK signaling, SIRT1, PGC-1α, streptozotocin-induced diabetes, neurodegeneration, diabetes mellitus
MeSH terms
Animals, Diabetes Mellitus, Experimental, Diabetic Neuropathies, Food, Humans, Mitochondria, Neurons, Rodentia, Proteome, Diabetes Complications

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