Evidence map›Paper›PMID 42410330›Full record

ArticleDiabetes, obesity & metabolism2026

Exercise Resistance in Obese Male NZO Mice Manifests as Local Muscle Remodelling Without Glycaemic Improvements.

Christian Springer, Sebastian Sill, Christian Binsch, Taylor Schoen, Laura Toska, Matthias Lienhard, Ralf Herwig, Stefan Börno, Bernd Timmermann, Diran Herebian and 9 more

Abstract read
In one paragraph

Article in Diabetes, obesity & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

19 authors.

Christian SpringerInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.
Sebastian SillInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.
Christian BinschInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.
Taylor SchoenInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.
Laura ToskaInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.
Matthias LienhardMax-Planck-Institute for Molecular Genetics, Berlin, Germany.
Ralf HerwigMax-Planck-Institute for Molecular Genetics, Berlin, Germany.
Stefan BörnoMax-Planck-Institute for Molecular Genetics, Berlin, Germany.
Bernd TimmermannMax-Planck-Institute for Molecular Genetics, Berlin, Germany.
Diran HerebianDepartment of General Pediatrics, Neonatology and Pediatric Cardiology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
D Margriet OuwensInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.
Delsi AltenhofenInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.
Angelika HorrighsInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.
Birgit KnebelInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.
Regina EnsenauerDepartment of General Pediatrics, Neonatology and Pediatric Cardiology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Dominik PestaGerman Aerospace Center-DLR, Institute of Aerospace Medicine, Cologne, Germany.ORCID https://orcid.org/0000-0002-5089-3586
Michael RodenGerman Center for Diabetes Research, Partner Düsseldorf, München-Neuherberg, Germany.
Alexandra ChadtInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.ORCID https://orcid.org/0000-0003-3873-1477
Hadi Al-HasaniInstitute for Clinical Biochemistry and Pathobiochemistry, Leibniz Center for Diabetes Research at Heinrich Heine University, Medical Faculty, Düsseldorf, Germany.

Funding

EFSD/Novo Nordisk Programme for Diabetes Research, and the Deutsche Diabetes GesellschaftFederal Ministry of Health (BMG)German Diabetes Center (DDZ)German Research Foundation (DFG) DFG-RTG 2576 vividMinistry of Culture and Science of the State of North Rhine-Westphalia (MKW NRW)
6 · The paper itself

Abstract

aimsExercise improves glycaemic control, yet some individuals show limited benefit, termed exercise resistance. We investigated tissue-specific adaptations to chronic exercise in a polygenic model of obesity-driven type 2 diabetes (T2D). MATERIALS AND

methodsMale New Zealand Obese (NZO) mice were fed a high-fat diet and underwent 6 weeks of interval treadmill training. Physical capacity, body composition, glucose metabolism, skeletal muscle and liver glycogen and triglycerides, mitochondrial function, transcriptomics and systemic metabolites were assessed.

resultsThe training regime had a positive impact on several physiological parameters, including increased physical capacity (18%, p < 0.01), skeletal muscle AMPK phosphorylation (25%, p < 0.05), complex I-linked respiration (67%, p < 0.05) and transcriptomic enrichment of muscle contraction pathways in trained versus sedentary NZO mice. However, body weight, fat mass, fasting glycaemia, insulin-stimulated glucose uptake, AKT phosphorylation and GLUT4 abundance remained unaltered. Plasma branched-chain amino acids (BCAAs) and ketone bodies (3.3-fold higher in trained, p < 0.05) increased, hepatic triglycerides rose (25%, p < 0.001) with hepatic glycogen depletion (37%, p < 0.05) and caloric intake was slightly higher.

conclusionsInterval training induced muscle-specific remodelling and enhanced physical capacity without improving systemic insulin sensitivity. Persistent adiposity, exacerbated hepatic steatosis and elevated circulating BCAAs may contribute to limited glycaemic improvement, with altered energy balance as a possible confounder. Consequently, the NZO model offers translational insight into tissue-uncoupled exercise resistance observed in human polygenic obesity and T2D heterogeneity.

Indexed as

Blood GlucoseDiabetes Mellitus, Type 2Muscle, SkeletalObesityPhysical Conditioning, AnimalAnimalsDiet, High-FatDisease Models, AnimalInsulin ResistanceLiverMaleMiceMice, ObeseBlood Glucoseexercise resistanceinterval trainingmitochondrial adaptationobesityskeletal muscle metabolism

Identifiers

PMID42410330
PMCPMC13448886

What Socratic holds

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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 Socratic graph.