Evidence map›Paper›PMID 39983345›Full record

ArticleRedox biology2025

Multi-tissue metabolomics reveal mtDNA- and diet-specific metabolite profiles in a mouse model of cardiometabolic disease.

Abhishek Shastry, Mia S Wilkinson, Dalia M Miller, Michelle Kuriakose, Jennifer L M H Veeneman, Matthew Ryan Smith, Charles C T Hindmarch, Kimberly J Dunham-Snary

Abstract read
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In one paragraph

Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  5. Review
  6. Article
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

8 authors.

Abhishek ShastryDepartment of Medicine, Queen's University, Kingston, ON, K7L 3N6, Canada.
Mia S WilkinsonDepartment of Medicine, Queen's University, Kingston, ON, K7L 3N6, Canada.
Dalia M MillerDepartment of Medicine, Queen's University, Kingston, ON, K7L 3N6, Canada.
Michelle KuriakoseDepartment of Biomedical & Molecular Sciences, Queen's University, Kingston, ON, K7L 3N6, Canada.
Jennifer L M H VeenemanDepartment of Molecular Genetics, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Matthew Ryan SmithAtlanta Veterans Affairs Health Care System, Decatur, GA, 30033, USA; Department of Medicine, Emory University, Atlanta, GA, 30322, USA.
Charles C T HindmarchDepartment of Medicine, Queen's University, Kingston, ON, K7L 3N6, Canada; Department of Biomedical & Molecular Sciences, Queen's University, Kingston, ON, K7L 3N6, Canada; Queen's CardioPulmonary Unit, Queen's University, Kingston, ON, K7L 3N6, Canada.
Kimberly J Dunham-SnaryDepartment of Medicine, Queen's University, Kingston, ON, K7L 3N6, Canada; Department of Biomedical & Molecular Sciences, Queen's University, Kingston, ON, K7L 3N6, Canada. Electronic address: kimberly.dunhamsnary@queensu.ca.

Funding

BLRD VA IK2 BX005913
6 · The paper itself

Abstract

rationaleExcess consumption of sugar- and fat-rich foods has heightened the prevalence of cardiometabolic disease, which remains a driver of cardiovascular disease- and type II diabetes-related mortality globally. Skeletal muscle insulin resistance is an early feature of cardiometabolic disease and is a precursor to diabetes. Insulin resistance risk varies with self-reported race, whereby African-Americans have a greater risk of diabetes development relative to their White counterparts. Self-reported race is strongly associated with mitochondrial DNA (mtDNA) haplogroups, and previous reports have noted marked differences in bioenergetic and metabolic parameters in cells belonging to distinct mtDNA haplogroups, but the mechanism of these associations remains unknown. Additionally, distinguishing nuclear DNA (nDNA) and mtDNA contributions to cardiometabolic disease remains challenging in humans. The Mitochondrial-Nuclear eXchange (MNX) mouse model enables in vivo preclinical investigation of the role of mtDNA in cardiometabolic disease development, and has been implemented in studies of insulin resistance, fatty liver disease, and obesity in previous reports.

methodsSix-week-old male C57

resultsComparative analyses between nDNA-matched wild-type and MNX strains demonstrated significantly increased body fat percentage in mice possessing C57

conclusionsThese results reveal novel nDNA-mtDNA interactions that drive significant changes in metabolite levels. Alterations to key metabolites involved in mitochondrial bioenergetic dysfunction and electron transport chain activity are implicated in elevated beta-oxidation during high-fat diet feeding; abnormally elevated rates of beta-oxidation may be a key driver of insulin resistance. The results reported here support the hypothesis that mtDNA influences cardiometabolic disease-susceptibility by modulating mitochondrial function and metabolic pathways.

Indexed as

Cardiovascular DiseasesDNA, MitochondrialMetabolomeMetabolomicsAnimalsDietDisease Models, AnimalHumansInsulin ResistanceMaleMiceMice, Inbred C57BLMuscle, SkeletalDNA, MitochondrialCardiometabolic diseaseDisease susceptibilityMetabolomicsMitochondrial geneticsMitochondrial-nuclear eXchangePlasmaSkeletal muscle

Identifiers

PMID39983345
PMCPMC11893332

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Registered trials

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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.