Nutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetes
Open accessAbstract
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)
- PMC
- PMC3375692
- 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
- bronze
- doi.org
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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