Evidence map›Paper›PMID 33493548›Full record

ArticleMetabolism: clinical and experimental2021

Increased insulin sensitivity and diminished pancreatic beta-cell function in DNA repair deficient Ercc1

Ana P Huerta Guevara, Sara J McGowan, Melissa Kazantzis, Tania Rozgaja Stallons, Tokio Sano, Niels L Mulder, Angelika Jurdzinski, Theo H van Dijk, Bart J L Eggen, Johan W Jonker and 2 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Metabolism: clinical and experimental, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
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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 at 3 institutions in 2 countries.

Ana P Huerta GuevaraSection of Molecular Metabolism and Nutrition, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB Groningen, the Netherlands.
Sara J McGowanInstitute on the Biology of Aging and Metabolism and Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, 6-155 Jackson Hall, 321 Church St., Minneapolis, MN 55455, USA; Department of Metabolism and Aging, Scripps Research Institute, Jupiter, FL 33458, USA.
Melissa KazantzisMetabolic Core, Scripps Research Institute, Jupiter, FL 33458, USA.
Tania Rozgaja StallonsDepartment of Metabolism and Aging, Scripps Research Institute, Jupiter, FL 33458, USA.
Tokio SanoDepartment of Metabolism and Aging, Scripps Research Institute, Jupiter, FL 33458, USA.
Niels L MulderSection of Molecular Metabolism and Nutrition, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB Groningen, the Netherlands.
Angelika JurdzinskiSection of Molecular Metabolism and Nutrition, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB Groningen, the Netherlands.
Theo H van DijkLaboratory Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB Groningen, the Netherlands.
Bart J L EggenDepartment of Biomedical Sciences of Cells & Systems, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB Groningen, the Netherlands.
Johan W JonkerSection of Molecular Metabolism and Nutrition, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB Groningen, the Netherlands.
Laura J NiedernhoferInstitute on the Biology of Aging and Metabolism and Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, 6-155 Jackson Hall, 321 Church St., Minneapolis, MN 55455, USA; Department of Metabolism and Aging, Scripps Research Institute, Jupiter, FL 33458, USA.
Janine K KruitSection of Molecular Metabolism and Nutrition, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB Groningen, the Netherlands. Electronic address: j.k.kruit@umcg.nl.
Scripps Research Institute · USUniversity Medical Center Groningen · NLUniversity of Groningen · NL

Funding

Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla, Nathan K LeBrasseur · 2019 to 2026
$28.7M
Validation and characterization of the identified variants associated with human longevity in mouse modelsU19AG056278 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI NIR J BARZILAI, Paul D. Robbins · 2017 to 2026
$24.5M
PROTEOMICSP01AG043376 · NIA · UNIVERSITY OF MINNESOTA · PI ROBBINS, PAUL D. · 2013 to 2019
$11.2M
Using the senolytic fisetin to suppress mortality in aged mice acutely exposed to murine beta-coronavirusR01AG063543 · NIA · UNIVERSITY OF MINNESOTA · PI NIEDERNHOFER, LAURA JANE · 2019 to 2023
$3.4M
NIA NIH HHS P01 AG043376NIA NIH HHS P01 AG062413NIA NIH HHS R01 AG063543NIA NIH HHS U19 AG056278
6 · The paper itself

Abstract

backgroundType 2 diabetes (T2DM) is an age-associated disease characterized by hyperglycemia due to insulin resistance and decreased beta-cell function. DNA damage accumulation has been associated with T2DM, but whether DNA damage plays a role in the pathogenesis of the disease is unclear. Here, we used mice deficient for the DNA excision-repair gene Ercc1 to study the impact of persistent endogenous DNA damage accumulation on energy metabolism, glucose homeostasis and beta-cell function.

methodsERCC1-XPF is an endonuclease required for multiple DNA repair pathways and reduced expression of ERCC1-XPF causes accelerated accumulation of unrepaired endogenous DNA damage and accelerated aging in humans and mice. In this study, energy metabolism, glucose metabolism, beta-cell function and insulin sensitivity were studied in Ercc1

resultsErcc1

conclusionSpontaneous DNA damage accumulation triggers an adaptive response resulting in improved insulin sensitivity. Loss of DNA repair, however, does negatively impacts beta-cell survival and function in Ercc1

Indexed as

AgingAnimalsApoptosisCell SurvivalDiabetes Mellitus, Type 2DNA-Binding ProteinsDNA DamageDNA RepairEndonucleasesGlucoseInsulinInsulin ResistanceInsulin-Secreting CellsMaleMiceMice, Inbred C57BLDNA-Binding ProteinsEndonucleasesErcc1 protein, mouseGlucoseInsulinBeta-cell functionDNA repairEnergy metabolismGenotoxic stressGlucose homeostasisSomatotropic axis

Identifiers

PMID33493548
PMCPMC8625516
OpenAlexW3124793622

What OpenQuestion holds

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LicenceCC BY
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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.