Evidence map›Paper›PMID 31217350›Full record

ArticleJCI insight2019

The combination of loss of glyoxalase1 and obesity results in hyperglycemia.

Elisabeth Lodd, Lucas M Wiggenhauser, Jakob Morgenstern, Thomas H Fleming, Gernot Poschet, Michael Büttner, Christoph T Tabler, David P Wohlfart, Peter P Nawroth, Jens Kroll

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  5. Glyoxalase 1 is a proadipogenic gene.The Journal of biological chemistry · 2025
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  6. Review
  7. Article
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  18. Analysis of the morphology of retinal vascular cells in zebrafish (Frontiers in cell and developmental biology · 2023
    Article
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  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

10 authors at 3 institutions in 1 country.

Elisabeth LoddDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Lucas M WiggenhauserDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Jakob MorgensternDepartment of Internal Medicine I and Clinical Chemistry, Heidelberg University Hospital, Heidelberg, Germany.
Thomas H FlemingDepartment of Internal Medicine I and Clinical Chemistry, Heidelberg University Hospital, Heidelberg, Germany.
Gernot PoschetMetabolomics Core Technology Platform, Centre for Organismal Studies, Heidelberg University, Heidelberg, Germany.
Michael BüttnerMetabolomics Core Technology Platform, Centre for Organismal Studies, Heidelberg University, Heidelberg, Germany.
Christoph T TablerDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
David P WohlfartDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Peter P NawrothDepartment of Internal Medicine I and Clinical Chemistry, Heidelberg University Hospital, Heidelberg, Germany.
Jens KrollDepartment of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Heidelberg University · DEUniversity Hospital Heidelberg · DEGerman Center for Diabetes Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increased formation of methylglyoxal (MG) under hyperglycemia is associated with the development of microvascular complications in patients with diabetes mellitus; however, the effects of elevated MG levels in vivo are poorly understood. In zebrafish, a transient knockdown of glyoxalase 1, the main MG detoxifying system, led to the elevation of endogenous MG levels and blood vessel alterations. To evaluate effects of a permanent knockout of glyoxalase 1 in vivo, glo1-/- zebrafish mutants were generated using CRISPR/Cas9. In addition, a diet-induced-obesity zebrafish model was used to analyze glo1-/- zebrafish under high nutrient intake. Glo1-/- zebrafish survived until adulthood without growth deficit and showed increased tissue MG concentrations. Impaired glucose tolerance developed in adult glo1-/- zebrafish and was indicated by increased postprandial blood glucose levels and postprandial S6 kinase activation. Challenged by an overfeeding period, fasting blood glucose levels in glo1-/- zebrafish were increased which translated into retinal blood vessel alterations. Thus, the data have identified a defective MG detoxification as a metabolic prerequisite and glyoxalase 1 alterations as a genetic susceptibility to the development of type 2 diabetes mellitus under high nutrition intake.

Indexed as

AnimalsCRISPR-Cas SystemsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2DietDisease Models, AnimalGene Knockout TechniquesGenetic Predisposition to DiseaseGlucoseHyperglycemiaInsulin ResistanceLactoylglutathione LyaseLiverMaleObesityPyruvaldehydeGlucoseLactoylglutathione LyasePyruvaldehydeDiabetesEndocrinologyMetabolism

Identifiers

PMID31217350
PMCPMC6629122
OpenAlexW2952589636

What OpenQuestion holds

Textmetadata
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.