Evidence map›Paper›PMID 20103706›Full record

ArticleDiabetes2010

Mitochondrial respiratory chain dysfunction in dorsal root ganglia of streptozotocin-induced diabetic rats and its correction by insulin treatment.

Subir K Roy Chowdhury, Elena Zherebitskaya, Darrell R Smith, Eli Akude, Sharmila Chattopadhyay, Corinne G Jolivalt, Nigel A Calcutt, Paul Fernyhough

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
7.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

79 citing papers in PubMed, 140 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Role of Mitochondrial Dysfunction in Neuropathy.International journal of molecular sciences · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Anti-Glucotoxicity Effect of PhytoconstituentsInternational journal of molecular sciences · 2023
    Review
  15. Peripheral mechanisms of peripheral neuropathic pain.Frontiers in molecular neuroscience · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Subir K Roy ChowdhuryDivision of Neurodegenerative Disorders, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada. skr_chowdhury@yahoo.ca
Elena Zherebitskaya
Darrell R Smith
Eli Akude
Sharmila Chattopadhyay
Corinne G Jolivalt
Nigel A Calcutt
Paul Fernyhough
St. Boniface Hospital · CAUniversity of California, San Diego · USUniversity of Manitoba · CA

Funding

Mechanisms of Spinally-Mediated Hyperalgesia in DiabetesR01DK057629 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CALCUTT, NIGEL A. · 2003 to 2011
$2.4M
CIHR 84214CIHR MOP-84214CIHR ROP-72893NIDDK NIH HHS DK057629NIDDK NIH HHS R01 DK057629
6 · The paper itself

Abstract

objectiveImpairments in mitochondrial physiology may play a role in diabetic sensory neuropathy. We tested the hypothesis that mitochondrial dysfunction in sensory neurons is due to abnormal mitochondrial respiratory function. RESEARCH DESIGN AND

methodsRates of oxygen consumption were measured in mitochondria from dorsal root ganglia (DRG) of 12- to- 22-week streptozotocin (STZ)-induced diabetic rats, diabetic rats treated with insulin, and age-matched controls. Activities and expression of components of mitochondrial complexes and reactive oxygen species (ROS) were analyzed.

resultsRates of coupled respiration with pyruvate + malate (P + M) and with ascorbate + TMPD (Asc + TMPD) in DRG were unchanged after 12 weeks of diabetes. By 22 weeks of diabetes, respiration with P + M was significantly decreased by 31-44% and with Asc + TMPD by 29-39% compared with control. Attenuated mitochondrial respiratory activity of STZ-diabetic rats was significantly improved by insulin that did not correct other indices of diabetes. Activities of mitochondrial complexes I and IV and the Krebs cycle enzyme, citrate synthase, were decreased in mitochondria from DRG of 22-week STZ-diabetic rats compared with control. ROS levels in perikarya of DRG neurons were not altered by diabetes, but ROS generation from mitochondria treated with antimycin A was diminished compared with control. Reduced mitochondrial respiratory function was associated with downregulation of expression of mitochondrial proteins.

conclusionsMitochondrial dysfunction in sensory neurons from type 1 diabetic rats is associated with impaired rates of respiratory activity and occurs without a significant rise in perikaryal ROS.

Indexed as

AnimalsCitrate (si)-SynthaseDiabetes Mellitus, ExperimentalDiabetic NeuropathiesGanglia, SpinalHypoglycemic AgentsInsulinMaleMitochondriaOxygen ConsumptionRatsRats, Sprague-DawleyReactive Oxygen SpeciesCitrate (si)-SynthaseHypoglycemic AgentsInsulinReactive Oxygen Species

Identifiers

PMID20103706
PMCPMC2844817
OpenAlexW2105042598

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.