Evidence map›Paper›PMID 41101703›Full record

ArticleJournal of sport and health science2025

Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice.

Nimna Perera, Minh Deo, Surafel Tegegne, Yow Keat Tham, Natalie A Mellett, Anida Velagic, Alex M Parker, Oliver K Fuller, Lauren V Terry, Casey L Egan and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of sport and health science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

14 authors.

Nimna PereraDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.
Minh DeoDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.
Surafel TegegneDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.
Yow Keat ThamBaker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia; Department of Diabetes, Central Clinical School, Monash University, Clayton, VIC 3800, Australia; Department of Cardiometabolic Health, University of Melbourne, Melbourne, VIC 3010, Australia.
Natalie A MellettBaker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Anida VelagicDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.
Alex M ParkerDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.
Oliver K FullerDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.
Lauren V TerryDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.
Casey L EganDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia.
Peter J MeikleBaker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Rebecca H RitchieDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia; Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Mark A FebbraioDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia. Electronic address: mark.febbraio@monash.edu.
Miles J De BlasioDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia; Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia. Electronic address: miles.deblasio@monash.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity is a risk factor for developing cardiometabolic disease. Exercise training is pivotal in the treatment of obesity and is associated with reduced cardiovascular mortality. This study examined the effect of high-fat feeding on cardiac morphology and mitochondrial function, alongside the mitigating effects of voluntary exercise training.

methodsSix-week-old male C57Bl/6 J mice commenced a high fat diet (HFD) or chow diet and were randomized to receive locked (sedentary) or unlocked (voluntary exercise training (VET)) running wheels at 10 weeks of age. Mice were monitored until 30 weeks of age and euthanized for collection of tissues. Magnetic resonance imaging was performed to assess body composition, and echocardiography was performed to assess cardiac function.

resultsCompared with chow-fed animals, the HFD increased body weight and adiposity and decreased cardiolipins (CL) in the heart, which are required for maintaining adequate mitochondrial respiration. Importantly, VET reversed these effects and induced physiological cardiac hypertrophy. Cardiac mitochondrial respiratory chain analysis revealed decreased complexes II and IV activity following high fat feeding, while VET enhanced complex I activity, emphasizing the cardioprotective effect of exercise training in obesity.

conclusionThis study uncovers mechanisms by which obesity and exercise impact cardiac mitochondrial health and suggests the mitochondria is a therapeutic target in obesity-related cardiovascular diseases.

Indexed as

CardiolipinCardiovascular diseaseExercise trainingMitochondriaObesity

Identifiers

PMID41101703
PMCPMC12811436

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.