Evidence map›Paper›PMID 38238601›Full record

ArticleNature aging2024

Gpcpd1-GPC metabolic pathway is dysfunctional in aging and its deficiency severely perturbs glucose metabolism.

Domagoj Cikes, Michael Leutner, Shane J F Cronin, Maria Novatchkova, Lorenz Pfleger, Radka Klepochová, Benjamin Lair, Marlène Lac, Camille Bergoglio, Nathalie Viguerie and 15 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
6.5field-weighted citation impact, top 3% of its field
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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
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  3. Review
  4. Observational
  5. Engineering Microbial Particles for Next-Generation Biomedical Platforms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025
    Review
  11. Review
  12. Metabolomics and Gut Microbiota in Elderly Patients with Diabetic Peripheral Neuropathy and Sarcopenia.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Article
  13. Article
  14. Article
  15. 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

25 authors at 8 institutions in 5 countries.

Domagoj CikesInstitute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria. domagoj.cikes@jku.at.ORCID http://orcid.org/0000-0003-0350-5672
Michael LeutnerDivision of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Shane J F CroninInstitute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.
Maria NovatchkovaInstitute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.
Lorenz PflegerDivision of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0003-1268-9565
Radka KlepochováDivision of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Benjamin LairTeam MetaDiab, Inserm UMR1297, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Marlène LacTeam MetaDiab, Inserm UMR1297, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Camille BergoglioTeam MetaDiab, Inserm UMR1297, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.ORCID http://orcid.org/0000-0003-1394-7677
Nathalie ViguerieTeam MetaDiab, Inserm UMR1297, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.ORCID http://orcid.org/0000-0002-1730-9915
Gerhard DürnbergerVienna Biocenter Core Facilities, Vienna Biocenter, Vienna, Austria.
Elisabeth RoitingerVienna Biocenter Core Facilities, Vienna Biocenter, Vienna, Austria.ORCID http://orcid.org/0000-0002-3405-7801
Mihaela GrivejVienna Biocenter Core Facilities, Vienna Biocenter, Vienna, Austria.
Eric RullmanDivision of Clinical Physiology, Department of Laboratory Medicine, Karolinska Institutet, and Unit of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-2854-7262
Thomas GustafssonDivision of Clinical Physiology, Department of Laboratory Medicine, Karolinska Institutet, and Unit of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.
Astrid HagelkruysInstitute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.
Geneviève TavernierTeam MetaDiab, Inserm UMR1297, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Virginie BourlierTeam MetaDiab, Inserm UMR1297, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Claude KnaufINSERM U1220 Institut de Recherche en Santé Digestive, CHU Purpan, Université Toulouse III Paul Sabatier Toulouse, Toulouse, France.ORCID http://orcid.org/0000-0001-5213-5378
Michael KrebsDivision of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Alexandra Kautzky-WillerDivision of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Cedric MoroTeam MetaDiab, Inserm UMR1297, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.ORCID http://orcid.org/0000-0003-4294-0597
Martin KrssakDivision of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Michael OrthoferInstitute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria.
Josef M PenningerInstitute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria. josef.penninger@helmholtz-hzi.de.ORCID http://orcid.org/0000-0002-8194-3777
Inserm · FRMedical University of Vienna · ATInstitute of Molecular Biotechnology · ATVienna Biocenter · ATKarolinska University Hospital · SEAustrian Academy of Sciences · ATJohannes Kepler University of Linz · ATUniversité Toulouse III - Paul Sabatier · FR

Funding

Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) KLI-904-B
6 · The paper itself

Abstract

Skeletal muscle plays a central role in the regulation of systemic metabolism during lifespan. With aging, this function is perturbed, initiating multiple chronic diseases. Our knowledge of mechanisms responsible for this decline is limited. Glycerophosphocholine phosphodiesterase 1 (Gpcpd1) is a highly abundant muscle enzyme that hydrolyzes glycerophosphocholine (GPC). The physiological functions of Gpcpd1 remain largely unknown. Here we show, in mice, that the Gpcpd1-GPC metabolic pathway is perturbed in aged muscles. Further, muscle-specific, but not liver- or fat-specific, inactivation of Gpcpd1 resulted in severely impaired glucose metabolism. Western-type diets markedly worsened this condition. Mechanistically, Gpcpd1 muscle deficiency resulted in accumulation of GPC, causing an 'aged-like' transcriptomic signature and impaired insulin signaling in young Gpcpd1-deficient muscles. Finally, we report that the muscle GPC levels are markedly altered in both aged humans and patients with type 2 diabetes, displaying a high positive correlation between GPC levels and chronological age. Our findings reveal that the muscle GPCPD1-GPC metabolic pathway has an important role in the regulation of glucose homeostasis and that it is impaired during aging, which may contribute to glucose intolerance in aging.

Indexed as

Diabetes Mellitus, Type 2GlucoseGlycerylphosphorylcholinePhospholipasesAgedAgingAnimalsHumansMetabolic Networks and PathwaysMiceMuscle, SkeletalGlucoseGlycerylphosphorylcholineGPCPD1 protein, humanPhospholipases

Identifiers

PMID38238601
OpenAlexW4390975733

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.