Evidence map›Paper›PMID 22201551›Full record

ArticleExperimental neurology2012

Protection from diabetes-induced peripheral sensory neuropathy--a role for elevated glyoxalase I?

M M Jack, J M Ryals, D E Wright

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Abnormal Intraepidermal Nerve Fiber Density in Disease: A Scoping Review.medRxiv : the preprint server for health sciences · 2023
    Article
  7. Article
  8. Vescalagin from Pink Wax Apple (Plants (Basel, Switzerland) · 2021
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Methylglyoxal-Glyoxalase 1 Balance: The Root of Vascular Damage.International journal of molecular sciences · 2017
    Review
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

3 authors at 1 institution in 1 country.

M M JackDepartment of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
J M Ryals
D E Wright
University of Kansas Medical Center · US

Funding

Research Design and Analysis Core (RDAC)P30HD002528 · NICHD · UNIVERSITY OF KANSAS LAWRENCE · PI COLOMBO, JOHN A. · 1985 to 2015
$22.1M
Painful Versus Insensate Diabetic NeuropathyR01NS043314 · NINDS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Douglas E Wright · 2003 to 2026
$6.7M
NICHD NIH HHS P30 HD 002528NICHD NIH HHS P30 HD002528NINDS NIH HHS R01 NS043314NINDS NIH HHS R01NS43314
6 · The paper itself

Abstract

Diabetic neuropathy is a common complication of diabetes mellitus with over half of all patients developing neuropathy symptoms due to sensory nerve damage. Diabetes-induced hyperglycemia leads to the accelerated production of advanced glycation end products (AGEs) that alter proteins, thereby leading to neuronal dysfunction. The glyoxalase enzyme system, specifically glyoxalase I (GLO1), is responsible for detoxifying precursors of AGEs, such as methylglyoxal and other reactive dicarbonyls. The purpose of our studies was to determine if expression differences of GLO1 may play a role in the development of diabetic sensory neuropathy. BALB/cJ mice naturally express low levels of GLO1, while BALB/cByJ express approximately 10-fold higher levels on a similar genetic background due to increased copy numbers of GLO1. Five weeks following STZ injection, diabetic BALB/cJ mice developed a 68% increase in mechanical thresholds, characteristic of insensate neuropathy or loss of mechanical sensitivity. This behavior change correlated with a 38% reduction in intraepidermal nerve fiber density (IENFD). Diabetic BALB/cJ mice also had reduced expression of mitochondrial oxidative phosphorylation proteins in Complexes I and V by 83% and 47%, respectively. Conversely, diabetic BALB/cByJ mice did not develop signs of neuropathy, changes in IENFD, or alterations in mitochondrial protein expression. Reduced expression of GLO1 paired with diabetes-induced hyperglycemia may lead to neuronal mitochondrial damage and symptoms of diabetic neuropathy. Therefore, AGEs, the glyoxalase system, and mitochondrial dysfunction may play a role in the development and modulation of diabetic peripheral neuropathy.

Indexed as

Analysis of VarianceAnimalsBlood GlucoseBody WeightDiabetic NeuropathiesDisease Models, AnimalGene Expression Regulation, EnzymologicLactoylglutathione LyaseMaleMiceMice, Inbred BALB CMitochondrial DiseasesMultienzyme ComplexesNerve FibersNeural ConductionPain MeasurementBlood GlucoseLactoylglutathione LyaseMultienzyme ComplexesStreptozocin

Identifiers

PMID22201551
PMCPMC3294099
OpenAlexW2009472247

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.