Evidence map›Paper›PMID 29893744›Full record

ArticleThe Journal of clinical investigation2018

Galactose protects against cell damage in mouse models of acute pancreatitis.

Shuang Peng, Julia V Gerasimenko, Tetyana M Tsugorka, Oleksiy Gryshchenko, Sujith Samarasinghe, Ole H Petersen, Oleg V Gerasimenko

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.3field-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

25 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Phosphate Improves Mitochondrial Function and Reduces Pancreatitis in Hypertriglyceridemia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. The role of CaCell calcium · 2023
    Review
  12. Upregulation of the ERRγ-VDAC1 axis underlies the molecular pathogenesis of pancreatitis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. The 2022 George E Palade Medal Lecture: Toxic CaPancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2023
    Review
  17. A microRNA checkpoint for CaMolecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Shuang PengCardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Julia V GerasimenkoCardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Tetyana M TsugorkaCardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Oleksiy GryshchenkoCardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Sujith SamarasingheGreat Ormond Street Hospital for Children, NHS Foundation Trust, London, United Kingdom.
Ole H PetersenCardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Oleg V GerasimenkoCardiff School of Biosciences, Cardiff University, Cardiff, United Kingdom.
Cardiff University · GBBogomoletz Institute of Physiology · UAGreat Ormond Street Hospital for Children NHS Foundation Trust · GBJinan University · CN

Funding

Medical Research Council MR/J002771/1
6 · The paper itself

Abstract

Acute pancreatitis (AP), a human disease in which the pancreas digests itself, has substantial mortality with no specific therapy. The major causes of AP are alcohol abuse and gallstone complications, but it also occurs as an important side effect of the standard asparaginase-based therapy for childhood acute lymphoblastic leukemia. Previous investigations into the mechanisms underlying pancreatic acinar cell death induced by alcohol metabolites, bile acids, or asparaginase indicated that loss of intracellular ATP generation is an important factor. We now report that, in isolated mouse pancreatic acinar cells or cell clusters, removal of extracellular glucose had little effect on this ATP loss, suggesting that glucose metabolism was severely inhibited under these conditions. Surprisingly, we show that replacing glucose with galactose prevented or markedly reduced the loss of ATP and any subsequent necrosis. Addition of pyruvate had a similar protective effect. We also studied the effect of galactose in vivo in mouse models of AP induced either by a combination of fatty acids and ethanol or asparaginase. In both cases, galactose markedly reduced acinar necrosis and inflammation. Based on these data, we suggest that galactose feeding may be used to protect against AP.

Indexed as

Acinar CellsAdenosine TriphosphateAnimalsAsparaginaseDisease Models, AnimalEthanolGalactoseHexokinaseHumansMiceMice, Inbred C57BLNecrosisPancreasPancreatitisPyruvic AcidAdenosine TriphosphateAsparaginaseEthanolGalactoseHexokinasePyruvic AcidCalcium signalingGastroenterologyLeukemiasOncology

Identifiers

PMID29893744
PMCPMC6118583
OpenAlexW2808521370

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.