Evidence map›Paper›PMID 19889414›Full record

ArticleAtherosclerosis2010

Association of telomere length with type 2 diabetes, oxidative stress and UCP2 gene variation.

Klelia D Salpea, Philippa J Talmud, Jackie A Cooper, Cecilia G Maubaret, Jeffrey W Stephens, Kavin Abelak, Steve E Humphries

Open access · greenAbstract read
In one paragraph

Article in Atherosclerosis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 5 pooled it
7.8field-weighted citation impact, top 2% 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

139 citing papers in PubMed, 5 syntheses or guidelines pooled it, 282 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Association between telomere length and diabetes mellitus: A meta-analysis.The Journal of international medical research · 2016
    Pooled it
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  6. Trial
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  10. Review
  11. Article
  12. Type 2 Diabetes From the Perspective of Telomere Biology.Endocrinology, diabetes & metabolism · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
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79 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 1 country.

Klelia D SalpeaCentre for Cardiovascular Genetics, Department of Medicine, British Heart Foundation Laboratories, Rayne Building, Royal Free and University College Medical School, 5 University Street, London, UK. k.salpea@ucl.ac.uk
Philippa J Talmud
Jackie A Cooper
Cecilia G Maubaret
Jeffrey W Stephens
Kavin Abelak
Steve E Humphries
British Heart Foundation · GBThe Royal Free Hospital · GBUniversity College London · GBSwansea University · GB

Funding

British Heart Foundation FS/06/053British Heart Foundation RG/08/008/25291British Heart Foundation RG2005/014
6 · The paper itself

Abstract

objectiveHigh oxidative stress potentially leads to accelerated telomere shortening and consequent premature cell senescence, implicated in type 2 diabetes (T2D) development. Therefore, we studied the association of leukocyte telomere length (LTL) with the presence of T2D, as well as the effect on the patients' LTL of plasma oxidative stress and of variation in UCP2, a gene involved in the mitochondrial production of reactive oxygen species.

methodsMean LTL was determined in 569 Caucasian, 103 South Asian and 70 Afro-Caribbean T2D patients aged from 24 to 92 years, 81 healthy Caucasian male students aged from 18 to 28 years and 367 healthy Caucasian men aged from 40 to 61 years by real-time PCR. Plasma total antioxidant status (TAOS) was measured in the T2D patients by a photometric microassay. The patients were also genotyped for the UCP2 functional variants -866G>A and A55V.

resultsAfro-Carribeans had 510bp longer mean length compared to Caucasians (p<0.0001) and 500bp longer than South Asians (p=0.004). T2D subjects displayed shorter age-adjusted LTL compared to controls [6.94(6.8-7.03) vs. 7.72(7.53-7.9), p<0.001] with subjects in the middle and the lowest tertile of LTL having significantly higher odds ratios for T2D compared to those in the highest tertile [1.50(1.08-2.07) and 5.04(3.63-6.99), respectively, p<0.0001]. In the patients, LTL was correlated negatively with age (r=-0.18, p<0.0001) and positively with TAOS measures (r=0.12, p=0.01) after adjusting for age, while carriers of the UCP2 -866A allele had shorter age-adjusted LTL than common homozygotes [6.86(6.76-6.96)kb vs. 7.03(6.91-7.15)kb, p=0.04].

conclusionThe present data suggest that shorter LTL is associated with the presence of T2D and this could be partially attributed to the high oxidative stress in these patients. The association of the UCP2 functional promoter variant with the LTL implies a link between mitochondrial production of reactive oxygen species and shorter telomere length in T2D.

Indexed as

AdultAgedAged, 80 and overAsian PeopleCellular SenescenceCohort StudiesDiabetes Mellitus, Type 2FemaleHeterozygoteHumansIon ChannelsMaleMiddle AgedMitochondriaMitochondrial ProteinsOxidative StressIon ChannelsMitochondrial ProteinsReactive Oxygen SpeciesUCP2 protein, humanUncoupling Protein 2

Identifiers

PMID19889414
PMCPMC2839074
OpenAlexW2114919699

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.