Evidence map›Paper›PMID 42913790›Full record

ArticleMolecular metabolism2026

BMI-anchored transcriptomics uncovers oxidative and inflammatory poles of obesity heterogeneity.

Su Yin-Yuan, Bundalian Linnaeus, Chen Yin-Cheng, Gjermeni Erind, Gille Benedikt, Richter Sandy, Jasaszwili Mariami, Palma-Vera Sergio Eliseo, Hoffmann Anne, Ghosh Adhideb and 6 more

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Article in Molecular metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

16 authors.

Su Yin-YuanInstitute of Biomedical Informatics, National Yang Ming Chiao Tung University, Taipei, Taiwan; Institute for Clinical Genetics, University Hospital Carl Gustav Carus at TUD Dresden University of Technology and Faculty of Medicine of TUD Dresden University of Technology, Dresden, Germany; Center for Computational and Systems Biology, National Taiwan University, Taipei, Taiwan.
Bundalian LinnaeusInstitute for Clinical Genetics, University Hospital Carl Gustav Carus at TUD Dresden University of Technology and Faculty of Medicine of TUD Dresden University of Technology, Dresden, Germany; Institute for Human Genetics, Leipzig University Medical Center, Leipzig, Germany.
Chen Yin-ChengInstitute of Biomedical Informatics, National Yang Ming Chiao Tung University, Taipei, Taiwan; Institute for Clinical Genetics, University Hospital Carl Gustav Carus at TUD Dresden University of Technology and Faculty of Medicine of TUD Dresden University of Technology, Dresden, Germany.
Gjermeni ErindDepartment of Cardiac Rehabilitation, Falkenstein Clinic, Bad Schandau, Germany.
Gille BenediktResearch Institute for Farm Animal Biology (FBN), Dummerstorf, Germany.
Richter SandyCenter for Pediatric Research, Hospital for Children and Adolescents, Leipzig University, Leipzig, Germany.
Jasaszwili MariamiCenter for Pediatric Research, Hospital for Children and Adolescents, Leipzig University, Leipzig, Germany.
Palma-Vera Sergio EliseoResearch Institute for Farm Animal Biology (FBN), Dummerstorf, Germany.
Hoffmann AnneHelmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG), Helmholtz Center Munich at the Leipzig University and University of Leipzig Medical Center, Leipzig, Germany.
Ghosh AdhidebLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, ETH Zürich, Schwerzenbach, Switzerland.
Wolfrum ChristianLaboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, ETH Zürich, Schwerzenbach, Switzerland.
Blüher MatthiasHelmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG), Helmholtz Center Munich at the Leipzig University and University of Leipzig Medical Center, Leipzig, Germany; Leipzig University Medical Center, Divisions of Endocrinology and Nephrology, University of Leipzig, Leipzig, Germany; LeiCeM - Leipzig Center of Metabolism, Leipzig University, Leipzig, Germany.
Peleg ShahafResearch Institute for Farm Animal Biology (FBN), Dummerstorf, Germany.
Garten AntjeCenter for Pediatric Research, Hospital for Children and Adolescents, Leipzig University, Leipzig, Germany; German Center for Child and Adolescent Health (DZKJ), partner site Leipzig-Dresden, Germany.
Le Duc DianaInstitute for Clinical Genetics, University Hospital Carl Gustav Carus at TUD Dresden University of Technology and Faculty of Medicine of TUD Dresden University of Technology, Dresden, Germany; Institute for Human Genetics, Leipzig University Medical Center, Leipzig, Germany. Electronic address: chenching.lin@nycu.edu.tw.
Lin Chen-ChingInstitute of Biomedical Informatics, National Yang Ming Chiao Tung University, Taipei, Taiwan; Institute for Clinical Genetics, University Hospital Carl Gustav Carus at TUD Dresden University of Technology and Faculty of Medicine of TUD Dresden University of Technology, Dresden, Germany. Electronic address: diana.leduc@ukdd.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBMI remains the dominant clinical index of obesity, but does not resolve adipose molecular programs that distinguish metabolic resilience from vulnerability.

methodsAmong 1,479 available human visceral adipose RNA-seq profiles, 1,298 samples from individuals with BMI 30-60 were included in the primary modeling cohort. Using BMI as a phenotypic anchor, we fit a LASSO regression model to derive transcriptome-predicted BMI and applied the resulting BMI-anchored transcriptomic model to mouse selection lines with divergent obesity phenotypes. In humans, directional discordance between measured and predicted BMI was used to define transcriptome-derived metabolically healthy obesity-like (MHO-like) and metabolically unhealthy obesity-like (MUO-like) states and to characterize pathophysiologic variation beyond measured BMI.

resultsModel-selected genes converged on immune, metabolic, mitochondrial, growth, structural-remodeling, and proteostasis programs. Cross-species application showed that BMI-anchored transcriptomic scores more closely tracked adipose-tissue content than body-size condition factor, distinguishing lipid-anabolic and inflammatory features of obesity-prone DU6 mice from the oxidative-catabolic phenotype of DU6P mice characterized by increased muscle mass. Gene-level associations with the transcriptomic score mirrored DU6-associated expression changes, linking the cross-species axis to an obesity-vulnerable adipose state. In humans, MHO-like individuals showed enhanced mitochondrial energy-production programs and more favorable glycemic and lipid profiles, whereas MUO-like individuals showed stress-adaptive metabolic remodeling and greater cardiometabolic medication use. In a separate, non-overlapping validation cohort, projection onto the primary-cohort PCA space retained a signal associated with insulin resistance that remained essentially unchanged after adjustment for sex.

conclusionsThese findings support a conserved adipose transcriptomic axis linking oxidative metabolic resilience to healthier obesity and lipid-inflammatory remodeling to metabolic vulnerability.

Indexed as

Body Mass IndexObesityTranscriptomeAdipose TissueAdultAnimalsFemaleHumansInflammationIntra-Abdominal FatMaleMiceMiddle AgedOxidative StressAdipose tissue metabolismAdipose transcriptomicsBMI-Anchored transcriptomic modelCross-species modelObesityVisceral adipose tissue

Identifiers

PMID42913790
PMCPMC13744826

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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.