Evidence map›Paper›PMID 33592336›Full record

ArticleMolecular metabolism2021

Sensory neurons derived from diabetic rats exhibit deficits in functional glycolysis and ATP that are ameliorated by IGF-1.

Mohamad-Reza Aghanoori, Vicky Margulets, Darrell R Smith, Lorrie A Kirshenbaum, Daniel Gitler, Paul Fernyhough

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
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

6 authors at 3 institutions in 2 countries.

Mohamad-Reza AghanooriDivision of Neurodegenerative Disorders, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, MB, Canada; Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, MB, Canada.
Vicky MarguletsDepartment of Physiology & Pathophysiology, University of Manitoba, Winnipeg, MB, Canada.
Darrell R SmithDivision of Neurodegenerative Disorders, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, MB, Canada.
Lorrie A KirshenbaumDepartment of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, MB, Canada; Department of Physiology & Pathophysiology, University of Manitoba, Winnipeg, MB, Canada; Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, MB, Canada.
Daniel GitlerDepartment of Physiology and Cell Biology, Faculty of Health Sciences, and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Paul FernyhoughDivision of Neurodegenerative Disorders, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, MB, Canada; Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, MB, Canada. Electronic address: pfernyhough@sbrc.ca.
St. Boniface Hospital · CABen-Gurion University of the Negev · ILUniversity of Manitoba · CA

Funding

CIHR
6 · The paper itself

Abstract

objectiveThe distal dying-back of the longest nerve fibres is a hallmark of diabetic neuropathy, and impaired provision of energy in the form of adenosine triphosphate (ATP) may contribute to this neurodegenerative process. We hypothesised that energy supplementation via glycolysis and/or mitochondrial oxidative phosphorylation is compromised in cultured dorsal root ganglion (DRG) sensory neurons from diabetic rodents, thus contributing to axonal degeneration. Functional analysis of glycolysis and mitochondrial respiration and real-time measurement of ATP levels in live cells were our specific means to test this hypothesis.

methodsDRG neuron cultures from age-matched control or streptozotocin (STZ)-induced type 1 diabetic rats were used for in vitro studies. Three plasmids containing ATP biosensors of varying affinities were transfected into neurons to study endogenous ATP levels in real time. The Seahorse XF analyser was used for glycolysis and mitochondrial respiration measurements.

resultsFluorescence resonance energy transfer (FRET) efficiency (YFP/CFP ratio) of the ATP biosensors AT1.03 (low affinity) and AT1.03

conclusionWe provide the first functional evidence for decreased glycolytic capacity in DRG neurons derived from type 1 diabetic rats. IGF-1 protected against the loss of ATP supplies in DRG cell bodies and axons in neurons derived from diabetic rats by augmenting various parameters of glycolysis and mitochondrial respiration.

Indexed as

Adenosine TriphosphateAnimalsAxonsDiabetes Mellitus, ExperimentalDiabetic NeuropathiesGanglia, SpinalGlycolysisInsulin-Like Growth Factor IMaleMitochondriaNeuritesRatsRats, Sprague-DawleySensory Receptor CellsSignal TransductionStreptozocinAdenosine Triphosphateinsulin-like growth factor-1, ratInsulin-Like Growth Factor IStreptozocinATP biosensorsAxon regenerationBioenergeticsDiabetic neuropathyMitochondrial respirationNeurite outgrowth

Identifiers

PMID33592336
PMCPMC7940986
OpenAlexW3133158994

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.