Evidence map›Paper›PMID 21494549›Full record

ArticlePloS one2011

Acute regulation of cardiac metabolism by the hexosamine biosynthesis pathway and protein O-GlcNAcylation.

Boglárka Laczy, Norbert Fülöp, Arzu Onay-Besikci, Christine Des Rosiers, John C Chatham

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.0field-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

43 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
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  3. Article
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  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. ProteinMetabolites · 2022
    Review
  12. A nexus of lipid andFrontiers in endocrinology · 2022
    Review
  13. Article
  14. Circadian regulation of cardiac metabolism.The Journal of clinical investigation · 2021
    Review
  15. Review
  16. Role ofPhysiological reviews · 2021
    Review
  17. Review
  18. Article
  19. Regulation of cardiac O-GlcNAcylation: More than just nutrient availability.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Review
  20. 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

5 authors at 4 institutions in 4 countries.

Boglárka LaczyDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Norbert Fülöp
Arzu Onay-Besikci
Christine Des Rosiers
John C Chatham
University of Alabama at Birmingham · USAnkara University · TRMontreal Heart Institute · CASomogy Megyei Kaposi Mór Oktató Kórház · HU

Funding

TYPE 2 DIABETES AND CARDIAC DYSFUNCTIONR01HL067464 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C · 2000 to 2009
$1.9M
Mechanisms of glucosamine ischemic cardioprotectionR01HL079364 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C · 2006 to 2010
$1.9M
Protein O-GlcNAcylation and the regulation of cardiac functionR01HL101192 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C · 2010 to 2014
$1.5M
CIHR 9575NHLBI NIH HHS HL067464NHLBI NIH HHS HL079364NHLBI NIH HHS HL101192NHLBI NIH HHS R01 HL067464NHLBI NIH HHS R01 HL079364NHLBI NIH HHS R01 HL101192
6 · The paper itself

Abstract

objectiveThe hexosamine biosynthesis pathway (HBP) flux and protein O-linked N-acetyl-glucosamine (O-GlcNAc) levels have been implicated in mediating the adverse effects of diabetes in the cardiovascular system. Activation of these pathways with glucosamine has been shown to mimic some of the diabetes-induced functional and structural changes in the heart; however, the effect on cardiac metabolism is not known. Therefore, the primary goal of this study was to determine the effects of glucosamine on cardiac substrate utilization.

methodsIsolated rat hearts were perfused with glucosamine (0-10 mM) to increase HBP flux under normoxic conditions. Metabolic fluxes were determined by (13)C-NMR isotopomer analysis; UDP-GlcNAc a precursor of O-GlcNAc synthesis was assessed by HPLC and immunoblot analysis was used to determine O-GlcNAc levels, phospho- and total levels of AMPK and ACC, and membrane levels of FAT/CD36.

resultsGlucosamine caused a dose dependent increase in both UDP-GlcNAc and O-GlcNAc levels, which was associated with a significant increase in palmitate oxidation with a concomitant decrease in lactate and pyruvate oxidation. There was no effect of glucosamine on AMPK or ACC phosphorylation; however, membrane levels of the fatty acid transport protein FAT/CD36 were increased and preliminary studies suggest that FAT/CD36 is a potential target for O-GlcNAcylation. CONCLUSION/

interpretationThese data demonstrate that acute modulation of HBP and protein O-GlcNAcylation in the heart stimulates fatty acid oxidation, possibly by increasing plasma membrane levels of FAT/CD36, raising the intriguing possibility that the HBP and O-GlcNAc turnover represent a novel, glucose dependent mechanism for regulating cardiac metabolism.

Indexed as

Biosynthetic PathwaysAcetylglucosamineAMP-Activated Protein Kinase KinasesAnimalsCD36 AntigensCell MembraneGlycosylationHeart Function TestsImmunoblottingIn Vitro TechniquesMyocardiumOxidation-ReductionPerfusionPhosphorylationProtein KinasesProteinsAcetylglucosamineAMP-Activated Protein Kinase KinasesCD36 AntigensCd36 protein, ratProtein KinasesProteinsUridine Diphosphate N-Acetylglucosamine

Identifiers

PMID21494549
PMCPMC3073970
OpenAlexW2001050822

What OpenQuestion holds

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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.