Evidence map›Paper›PMID 17693571›Full record

ArticleGenome research2007

Direct linkage of mitochondrial genome variation to risk factors for type 2 diabetes in conplastic strains.

Michal Pravenec, Masaya Hyakukoku, Josef Houstek, Vaclav Zidek, Vladimir Landa, Petr Mlejnek, Ivan Miksik, Kristyna Dudová-Mothejzikova, Petr Pecina, Marek Vrbacky and 10 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Genome research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–field-weighted citation impact
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

39 citing papers in PubMed, 88 citations in OpenAlex.

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  10. Metabolic Syndrome and Associated Diseases: From the Bench to the Clinic.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Review
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

20 authors at 6 institutions in 3 countries.

Michal PravenecInstitute of Physiology, Academy of Sciences of the Czech Republic, Prague 142 20, Czech Republic.
Masaya Hyakukoku
Josef Houstek
Vaclav Zidek
Vladimir Landa
Petr Mlejnek
Ivan Miksik
Kristyna Dudová-Mothejzikova
Petr Pecina
Marek Vrbacky
Zdenek Drahota
Alena Vojtiskova
Tomas Mracek
Ludmila Kazdova
Olena Oliyarnyk
Jiaming Wang
Christopher Ho
Nathan Qi
Ken Sugimoto
Theodore Kurtz
Czech Academy of Sciences · CZUniversity of California, San Francisco · USInstitute of Clinical and Experimental Medicine · CZSapporo Medical University · JPThe University of Osaka · JPUniversity of Michigan · US

Funding

UNIQUE CARDIOVASCULAR RESPONSE TO STRESSORS AND LINKAGE WITH HYPERTENSIONP01HL035018 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PRINTZ, MORTON P · 1986 to 2007
$14.7M
NEW EXPERIMENTAL MODELS OF HYPERTENSIONR01HL056028 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KURTZ, THEODORE W · 1997 to 2012
$4.0M
WHY DO METABOLIC RISK FACTORS CLUSTER WITH HYPERTENSION?R01HL063709 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI KURTZ, THEODORE W · 2000 to 2003
$885k
NHLBI NIH HHS HL35018NHLBI NIH HHS HL56028NHLBI NIH HHS HL63709NHLBI NIH HHS P01 HL035018NHLBI NIH HHS R01 HL056028NHLBI NIH HHS R01 HL063709
6 · The paper itself

Abstract

Recently, the relationship of mitochondrial DNA (mtDNA) variants to metabolic risk factors for diabetes and other common diseases has begun to attract increasing attention. However, progress in this area has been limited because (1) the phenotypic effects of variation in the mitochondrial genome are difficult to isolate owing to confounding variation in the nuclear genome, imprinting phenomena, and environmental factors; and (2) few animal models have been available for directly investigating the effects of mtDNA variants on complex metabolic phenotypes in vivo. Substitution of different mitochondrial genomes on the same nuclear genetic background in conplastic strains provides a way to unambiguously isolate effects of the mitochondrial genome on complex traits. Here we show that conplastic strains of rats with identical nuclear genomes but divergent mitochondrial genomes that encode amino acid differences in proteins of oxidative phosphorylation exhibit differences in major metabolic risk factors for type 2 diabetes. These results (1) provide the first direct evidence linking naturally occurring variation in the mitochondrial genome, independent of variation in the nuclear genome and other confounding factors, to inherited variation in known risk factors for type 2 diabetes; and (2) establish that spontaneous variation in the mitochondrial genome per se can promote systemic metabolic disturbances relevant to the pathogenesis of common diseases.

Indexed as

Genetic VariationGenomeAmino Acid SubstitutionAnimalsBase SequenceDiabetes Mellitus, Type 2DNA, MitochondrialElectron Transport Complex IVGene DosageHaplotypesMaleMitochondriaPolymorphism, GeneticRatsRats, Inbred BNRats, Inbred SHRDNA, MitochondrialElectron Transport Complex IV

Identifiers

PMID17693571
PMCPMC1950900
OpenAlexW2165456329

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.