Evidence map›Paper›PMID 23950916›Full record

ArticlePloS one2013

Long-term artificial sweetener acesulfame potassium treatment alters neurometabolic functions in C57BL/6J mice.

Wei-na Cong, Rui Wang, Huan Cai, Caitlin M Daimon, Morten Scheibye-Knudsen, Vilhelm A Bohr, Rebecca Turkin, William H Wood, Kevin G Becker, Ruin Moaddel and 2 more

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Re-evaluation of acesulfame K (E 950) as food additive.EFSA journal. European Food Safety Authority · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Article
  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

12 authors.

Wei-na CongMetabolism Unit, Laboratory of Clinical Investigation, National Institute on Aging, Baltimore, Maryland, United States of America.
Rui Wang
Huan Cai
Caitlin M Daimon
Morten Scheibye-Knudsen
Vilhelm A Bohr
Rebecca Turkin
William H Wood
Kevin G Becker
Ruin Moaddel
Stuart Maudsley
Bronwen Martin

Funding

Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
CLINICAL PROJECT: A study of hormone-expressing taste cells: in vivo and in vitroZIAAG000291 · NIA · NATIONAL INSTITUTE ON AGING · PI EGAN, JOSEPHINE · 2009 to 2025
$5.2M
Intramural NIH HHS
6 · The paper itself

Abstract

With the prevalence of obesity, artificial, non-nutritive sweeteners have been widely used as dietary supplements that provide sweet taste without excessive caloric load. In order to better understand the overall actions of artificial sweeteners, especially when they are chronically used, we investigated the peripheral and central nervous system effects of protracted exposure to a widely used artificial sweetener, acesulfame K (ACK). We found that extended ACK exposure (40 weeks) in normal C57BL/6J mice demonstrated a moderate and limited influence on metabolic homeostasis, including altering fasting insulin and leptin levels, pancreatic islet size and lipid levels, without affecting insulin sensitivity and bodyweight. Interestingly, impaired cognitive memory functions (evaluated by Morris Water Maze and Novel Objective Preference tests) were found in ACK-treated C57BL/6J mice, while no differences in motor function and anxiety levels were detected. The generation of an ACK-induced neurological phenotype was associated with metabolic dysregulation (glycolysis inhibition and functional ATP depletion) and neurosynaptic abnormalities (dysregulation of TrkB-mediated BDNF and Akt/Erk-mediated cell growth/survival pathway) in hippocampal neurons. Our data suggest that chronic use of ACK could affect cognitive functions, potentially via altering neuro-metabolic functions in male C57BL/6J mice.

Indexed as

AnimalsBlotting, WesternCell Line, TumorCognitionEnergy MetabolismHippocampusHumansInsulinIslets of LangerhansLeptinMaleMaze LearningMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutacetosulfameInsulinLeptinReceptors, G-Protein-CoupledReceptor, trkBSweetening Agentstaste receptors, type 1Thiazines

Identifiers

PMID23950916
PMCPMC3737213

What OpenQuestion holds

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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.