Evidence map›Paper›PMID 19799964›Full record

ReviewMolecular and cellular endocrinology2010

Hexosamine flux, the O-GlcNAc modification, and the development of insulin resistance in adipocytes.

Chin Fen Teo, Edith E Wollaston-Hayden, Lance Wells

Abstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 81 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  6. Article
  7. Review
  8. Roles of Protein Post-Translational Modifications During Adipocyte Senescence.International journal of biological sciences · 2023
    Review
  9. Posttranslational modifications in diabetes: Mechanisms and functions.Reviews in endocrine & metabolic disorders · 2022
    Review
  10. Cells · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Role of YAP/TAZ in Energy Metabolism in the Heart.Journal of cardiovascular pharmacology · 2019
    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.

Chin Fen TeoComplex Carbohydrate Research Center and Department of Biochemistry and Molecular Biology, University of Georgia, 315 Riverbend Road, Athens, GA 30602, USA.
Edith E Wollaston-Hayden
Lance Wells
University of Georgia · US

Funding

Role of O-GlcNAc in Metabolic SignalingR01DK075069 · NIDDK · UNIVERSITY OF GEORGIA · PI WELLS, LANCE · 2007 to 2011
$1.4M
NIDDK NIH HHS 1R01DK075069NIDDK NIH HHS R01 DK075069
6 · The paper itself

Abstract

Excess flux through the hexosamine biosynthesis pathway in adipocytes is a fundamental cause of "glucose toxicity" and the development of insulin resistance that leads to type II diabetes. Adipose tissue-specific elevation in hexosamine flux in animal models recapitulates whole-body insulin-resistant phenotypes, and increased hexosamine flux in adipocyte cell culture models impairs insulin-stimulated glucose uptake. Many studies have been devoted to unveiling the molecular mechanisms in adipocytes in response to excess hexosamine flux-mediated insulin resistance. As a major downstream event consuming and incorporating the final product of the hexosamine biosynthesis pathway, dynamic and inducible O-GlcNAc modification is emerging as a modulator of insulin sensitivity in adipocytes. Given that O-GlcNAc is implicated in both insulin-mediated signal transduction and transcriptional events essential for adipocytokine secretion, direct functional studies to pinpoint the roles of O-GlcNAc in the development of insulin resistance via excess flux through hexosamine biosynthesis pathway are needed.

Indexed as

AcetylglucosamineAdipocytesAnimalsGlycosylationHexosaminesHumansInsulinInsulin ResistanceAcetylglucosamineHexosaminesInsulin

Identifiers

PMID19799964
PMCPMC2855202
OpenAlexW2053531649

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.