Evidence map›Paper›PMID 20851343›Full record

ArticleChemistry & biology2010

Inhibition of O-GlcNAcase using a potent and cell-permeable inhibitor does not induce insulin resistance in 3T3-L1 adipocytes.

Matthew S Macauley, Yuan He, Tracey M Gloster, Keith A Stubbs, Gideon J Davies, David J Vocadlo

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Chemistry & biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 67 citations in OpenAlex.

  1. Expansion of the diversity of dispersin scaffolds.Acta crystallographica. Section D, Structural biology · 2025
    Article
  2. Review
  3. Article
  4. O-GlcNAcylation in ischemic diseases.Frontiers in pharmacology · 2024
    Review
  5. Review
  6. Posttranslational modifications in diabetes: Mechanisms and functions.Reviews in endocrine & metabolic disorders · 2022
    Review
  7. Article
  8. Role ofPhysiological reviews · 2021
    Review
  9. Review
  10. Review
  11. Article
  12. O-Linked β-Clinical science (London, England : 1979) · 2018
    Review
  13. Review
  14. Protein O-GlcNAcylation: emerging mechanisms and functions.Nature reviews. Molecular cell biology · 2017
    Review
  15. Article
  16. Article
  17. O-GlcNAc-ylation in the Nuclear Pore Complex.Cellular and molecular bioengineering · 2016
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Matthew S MacauleyDepartment of Chemistry, Simon Fraser University, Burnaby, BC, Canada.
Yuan He
Tracey M Gloster
Keith A Stubbs
Gideon J Davies
David J Vocadlo
Simon Fraser University · CAUniversity of York · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F007124/1CIHRWellcome Trust 082572
6 · The paper itself

Abstract

To probe increased O-GlcNAc levels as an independent mechanism governing insulin resistance in 3T3-L1 adipocytes, a new class of O-GlcNAcase (OGA) inhibitor was studied. 6-Acetamido-6-deoxy-castanospermine (6-Ac-Cas) is a potent inhibitor of OGA. The structure of 6-Ac-Cas bound in the active site of an OGA homolog reveals structural features contributing to its potency. Treatment of 3T3-L1 adipocytes with 6-Ac-Cas increases O-GlcNAc levels in a dose-dependent manner. These increases in O-GlcNAc levels do not induce insulin resistance functionally, measured using a 2-deoxyglucose (2-DOG) uptake assay, or at the molecular level, determined by evaluating levels of phosphorylated IRS-1 and Akt. These results, and others described, provide a structural blueprint for improved inhibitors and collectively suggest that increased O-GlcNAc levels, brought about by inhibition of OGA, does not by itself cause insulin resistance in 3T3-L1 adipocytes.

Indexed as

3T3-L1 CellsAcetylglucosamineAdipocytesAnimalsbeta-N-AcetylhexosaminidasesBinding SitesCatalytic DomainCrystallography, X-RayDeoxyglucoseEnzyme InhibitorsHumansIndolizinesInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceMice6-acetamido-6-deoxycastanospermineAcetylglucosaminebeta-N-AcetylhexosaminidasesDeoxyglucoseEnzyme Inhibitorshexosaminidase CIndolizinesInsulinInsulin Receptor Substrate ProteinsIrs1 protein, mouseN-acetylglucosaminono-1,5-lactone O-(phenylcarbamoyl)oximeOximesPhenylcarbamatesProto-Oncogene Proteins c-akt

Identifiers

PMID20851343
PMCPMC2954295
OpenAlexW2028479688

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.