Evidence map›Paper›PMID 26951191›Full record

ArticleClinical and translational medicine2016

Shortened leukocyte telomere length in type 2 diabetes mellitus: genetic polymorphisms in mitochondrial uncoupling proteins and telomeric pathways.

Yuling Zhou, Zhixin Ning, Yvonne Lee, Brett D Hambly, Craig S McLachlan

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

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  7. The Influence ofJournal of clinical medicine · 2023
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  14. FTO associations with obesity and telomere length.Journal of biomedical science · 2017
    Review
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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

5 authors at 3 institutions in 1 country.

Yuling ZhouFaculty of Medicine, Rural Clinical School, University of New South Wales, Samuels Building, Level 3, Room 327, Sydney, 2052, Australia. zhouyuling20120901@gmail.com.
Zhixin NingFaculty of Medicine, Rural Clinical School, University of New South Wales, Samuels Building, Level 3, Room 327, Sydney, 2052, Australia. z.ning@student.unsw.edu.au.
Yvonne LeeFaculty of Medicine, Rural Clinical School, University of New South Wales, Samuels Building, Level 3, Room 327, Sydney, 2052, Australia. yvonne.lee3@yahoo.com.
Brett D HamblyDiscipline of Pathology, Bosch Institute, Sydney Medical School, University of Sydney, Sydney, Australia. brett.hambly@sydney.edu.au.
Craig S McLachlanFaculty of Medicine, Rural Clinical School, University of New South Wales, Samuels Building, Level 3, Room 327, Sydney, 2052, Australia. reperfusion@hotmail.com.
University of South Australia · AUUNSW Sydney · AUUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current debate in type 2 diabetes (T2DM) has focused on shortened leukocyte telomere length (LTL) as the result of a number of possible causes, including polymorphisms in mitochondrial uncoupling proteins (UCPs) leading to oxidative stress, telomere regulatory pathway gene polymorphisms, or as a direct result of associated cardiovascular complications inducing tissue organ inflammation and oxidative stress. There is evidence that a heritable shorter telomere trait is a risk factor for development of T2DM. This review discusses the contribution and balance of genetic regulation of UCPs and telomere pathways in the context of T2DM. We discuss genotypes that are well known to influence the shortening of LTL, in particular OBFC1 and telomerase genotypes such as TERC. Interestingly, the interaction between short telomeres and T2DM risk appears to involve mitochondrial dysfunction as an intermediate process. A hypothesis is presented that genetic heterogeneity within UCPs may directly affect oxidative stress that feeds back to influence the fine balance of telomere regulation, cell cycle regulation and diabetes risk and/or metabolic disease progression.

Indexed as

GeneticsTelomere-associated pathway genesTelomere lengthType 2 diabetesUncoupling protein polymorphisms

Identifiers

PMID26951191
PMCPMC4781821
OpenAlexW2296093596

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.