Evidence map›Paper›PMID 39261587›Full record

ArticleCommunications biology2024

Haplotype variability in mitochondrial rRNA predisposes to metabolic syndrome.

Petr Pecina, Kristýna Čunátová, Vilma Kaplanová, Guillermo Puertas-Frias, Jan Šilhavý, Kateřina Tauchmannová, Marek Vrbacký, Tomáš Čajka, Ondřej Gahura, Markéta Hlaváčková and 6 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
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

16 authors.

Petr PecinaLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Kristýna ČunátováLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.ORCID 0000-0001-9993-2040
Vilma KaplanováLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Guillermo Puertas-FriasLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.ORCID 0000-0003-0580-3833
Jan ŠilhavýLaboratory of Genetics of Model Diseases, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Kateřina TauchmannováLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Marek VrbackýLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Tomáš ČajkaLaboratory of Translational Metabolism, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.ORCID 0000-0002-9728-3355
Ondřej GahuraInstitute of Parasitology, Biology Centre, Czech Academy of Sciences, České Budějovice, Czech Republic.ORCID 0000-0002-2925-4763
Markéta HlaváčkováLaboratory of Developmental Cardiology, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Viktor StráneckýResearch Unit for Rare Diseases, Department of Pediatrics and Adolescent Medicine, 1st Faculty of Medicine, Charles University, Prague, Czech Republic.
Stanislav KmochResearch Unit for Rare Diseases, Department of Pediatrics and Adolescent Medicine, 1st Faculty of Medicine, Charles University, Prague, Czech Republic.
Michal PravenecLaboratory of Genetics of Model Diseases, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Josef HouštěkLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Tomáš MráčekLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic. tomas.mracek@fgu.cas.cz.ORCID 0000-0002-9492-0718
Alena PecinováLaboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic. alena.pecinova@fgu.cas.cz.ORCID 0000-0002-0204-7502

Funding

Ministerstvo Školství, Mládeže a Tělovýchovy (Ministry of Education, Youth and Sports) LM2023067Ministerstvo Školství, Mládeže a Tělovýchovy (Ministry of Education, Youth and Sports) LUAUS23095
6 · The paper itself

Abstract

Metabolic syndrome is a growing concern in developed societies and due to its polygenic nature, the genetic component is only slowly being elucidated. Common mitochondrial DNA sequence variants have been associated with symptoms of metabolic syndrome and may, therefore, be relevant players in the genetics of metabolic syndrome. We investigate the effect of mitochondrial sequence variation on the metabolic phenotype in conplastic rat strains with identical nuclear but unique mitochondrial genomes, challenged by high-fat diet. We find that the variation in mitochondrial rRNA sequence represents risk factor in the insulin resistance development, which is associated with diacylglycerols accumulation, induced by tissue-specific reduction of the oxidative capacity. These metabolic perturbations stem from the 12S rRNA sequence variation affecting mitochondrial ribosome assembly and translation. Our work demonstrates that physiological variation in mitochondrial rRNA might represent a relevant underlying factor in the progression of metabolic syndrome.

Indexed as

HaplotypesMetabolic SyndromeRNA, RibosomalAnimalsDiet, High-FatDNA, MitochondrialGenetic Predisposition to DiseaseInsulin ResistanceMaleMitochondriaRatsRNA, MitochondrialDNA, MitochondrialRNA, MitochondrialRNA, RibosomalRNA, ribosomal, 12S

Identifiers

PMID39261587
PMCPMC11391015

What Socratic 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 Socratic graph.