Evidence map›Paper›PMID 26049631›Full record

ReviewCurrent opinion in clinical nutrition and metabolic care2015

You are what you eat: O-linked N-acetylglucosamine in disease, development and epigenetics.

Stéphanie Olivier-Van Stichelen, John A Hanover

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in clinical nutrition and metabolic care, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. PerturbingCells · 2026
    Article
  3. Review
  4. Review
  5. Tissue-specificeLife · 2024
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. GANAB andInternational journal of molecular sciences · 2022
    Review
  11. Cells · 2022
    Review
  12. Article
  13. Targeting ProteinCells · 2022
    Review
  14. Brain on food: The neuroepigenetics of nutrition.Neurochemistry international · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. OGT suppresses S6K1-mediated macrophage inflammation and metabolic disturbance.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  20. 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

2 authors at 2 institutions in 1 country.

Stéphanie Olivier-Van StichelenNational Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, Bethesda, Maryland, USA.
John A Hanover
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Targeted disruption the enzymes of O-GlcNAc cycling: Animal models of DiseaseZIADK060101 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$25.7M
Enzymes of O-GlcNAc cycling linked to type-2 diabetes and neurodegenerationZIADK060103 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$20.8M
Calmodulin-driven Nuclear Trafficking linked to diabetes and insulin signalingZIADK060102 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$8.5M
Intramural NIH HHS Z99 DK999999
6 · The paper itself

Abstract

purpose of reviewThe O-linked N-acetylglucosamine (O-GlcNAc) modification is both responsive to nutrient availability and capable of altering intracellular cellular signalling. We summarize data defining a role for O-GlcNAcylation in metabolic homeostasis and epigenetic regulation of development in the intrauterine environment. RECENT

findingsO-GlcNAc transferase (OGT) catalyzes nutrient-driven O-GlcNAc addition and is subject to random X-inactivation. OGT plays key roles in growth factor signalling, stem cell biology, epigenetics and possibly imprinting. The O-GlcNAcase, which removes O-GlcNAc, is subject to tight regulation by higher order chromatin structure. O-GlcNAc cycling plays an important role in the intrauterine environment wherein OGT expression is an important biomarker of placental stress. SUMMARY: Regulation of O-GlcNAc cycling by X-inactivation, epigenetic regulation and nutrient-driven processes makes it an ideal candidate for a nutrient-dependent epigenetic regulator of human disease. In addition, O-GlcNAc cycling influences chromatin modifiers critical to the regulation and timing of normal development including the polycomb repression complex and the ten-eleven translocation proteins mediating DNA methyl cytosine demethylation. The pathway also impacts the hypothalamic-pituitary-adrenal axis critical to intrauterine programming influencing disease susceptibility in later life.

Indexed as

Epigenesis, GeneticFeeding BehaviorAcetylglucosamineAlzheimer DiseaseCardiovascular DiseasesChromatinChronic DiseaseDiabetes Mellitus, Type 2DietFemaleGene Expression RegulationGenetic LociGenomic ImprintingHomeostasisHumansHypothalamo-Hypophyseal SystemAcetylglucosamineChromatinN-AcetylglucosaminyltransferasesO-GlcNAc transferaseUDP-N-acetylglucosamine-peptide beta-N-acetylglucosaminyltransferase

Identifiers

PMID26049631
PMCPMC4479189
OpenAlexW2419316099

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.