Evidence map›Paper›PMID 42124647›Full record

ArticlebioRxiv : the preprint server for biology2026

15-PGDH Inhibition Overcomes Muscle Regenerative Deficit Seen With GLP1-Receptor Agonist-Induced Weight Loss.

Minas Nalbandian, Jameel Lone, Emmeran Le Moal, Ireh Kim, Yutong Kelly Li, Peggy Kraft, Meng Zhao, Kassie Kolacar, Zeyuan Zhang, Katrin J Svensson and 1 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Minas NalbandianBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, CA, USA.
Jameel LoneDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Emmeran Le MoalBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, CA, USA.
Ireh KimBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, CA, USA.
Yutong Kelly LiBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, CA, USA.
Peggy KraftBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, CA, USA.
Meng ZhaoDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Kassie KolacarBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, CA, USA.
Zeyuan ZhangDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Katrin J SvenssonDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-5376-5128
Helen M BlauBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, CA, USA.

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI Seung K Kim · 2017 to 2026
$19.5M
Mechanisms controlling fructose uptake and utilizationR01DK125260 · NIDDK · STANFORD UNIVERSITY · PI Katrin Jennifer Svensson · 2020 to 2026
$3.5M
Regulation of eicosanoid signaling lipids to improve skeletal muscle function and increase healthspan during agingR01AG069858 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2020 to 2023
$2.4M
Learning Regulatory Drivers of Chromatin and Expression Dynamics during Nuclear ReprogrammingR01HG009674 · NHGRI · STANFORD UNIVERSITY · PI BLAU, HELEN M, KUNDAJE, ANSHUL · 2017 to 2019
$2.1M
Investigating Isthmin as an adipose-to-muscle messenger that promotes muscle protein synthesisK99AR081618 · NIAMS · STANFORD UNIVERSITY · PI ZHAO, MENG · 2023 to 2024
$182k
NHGRI NIH HHS R01 HG009674NIAMS NIH HHS K99 AR081618NIA NIH HHS R01 AG069858NIDDK NIH HHS P30 DK116074NIDDK NIH HHS R01 DK125260
6 · The paper itself

Abstract

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), including long-acting semaglutide, are revolutionary anti-obesity therapies. However, emerging evidence indicates that weight loss may come at the expense of skeletal muscle mass, a tissue essential for mobility, metabolic regulation, and overall health. Here, we show that an inhibitor of the gerozyme 15-hydroxyprostaglandin dehydrogenase (PGDHi), which boosts PGE2 levels, increases skeletal muscle mass, strength, and regeneration in the presence of semaglutide. We find that in a high fat diet-induced mouse model of obesity, semaglutide alone induces significant loss of muscle mass, while retaining contractile function. However, muscle regeneration and recovery of strength post-injury are hindered by semaglutide. This regenerative deficit is due to impeded stem cell function, which is overcome if mice are treated with a combination of PGDHi and semaglutide. Our data show that GLP-1-mediated weight loss interferes with this key muscle-building function, which PGDHi co-treatment counteracts to promote proper muscle regeneration and restored strength.

Indexed as

15-PGDH (gerozyme)GLP-1 receptor agonistmuscle stem cellsSemaglutideskeletal muscle regeneration

Identifiers

PMID42124647
PMCPMC13160160

What OpenQuestion 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 OpenQuestion graph.