The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
GLP-1 regulates exercise endurance and skeletal muscle remodeling via GLP-1R/AMPK pathway
Open accessAbstract
Exercise-induced physical endurance enhancement and skeletal muscle remodeling can prevent and delay the development of multiple diseases, especially metabolic syndrome. Herein, the study explored the association between glucagon-like peptide-1 (GLP-1) secretion and exercise, and its effect on skeletal muscle remodeling to enhance endurance capacity. We found both acute exercise and short-term endurance training significantly increased the secretion of GLP-1 in mice. Recombinant adeno-associated virus (AAV) encoding Gcg (proglucagon) was used to induce the overexpression of GLP-1 in skeletal muscle of mice. Overexpression of GLP-1 in skeletal muscle enhanced endurance capacity. Meanwhile, glycogen synthesis, glucose uptake, type I fibers proportion, and mitochondrial biogenesis were augmented in GLP-1-AAV skeletal muscle. Furthermore, the in vitro experiment showed that exendin-4 (a GLP-1 receptor agonist) treatment remarkably promoted glucose uptake, type I fibers formation, and mitochondrial respiration. Mechanistically, the knockdown of AMPK could reverse the effects imposed by GLP-1R activation in vitro. Taken together, these results verify that GLP-1 regulates skeletal muscle remodeling to enhance exercise endurance possibly via GLP-1R signaling-mediated phosphorylation of AMPK.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The interaction between GLP-1 and its receptor GLP-1R initiates the AMPK signaling cascade within skeletal muscle tissue. This initiation precipitates a multitude of alterations in the cellular milieu, notably the augmentation of mitochondrial biogenesis-a mechanism responsible for the genesis of new mitochondria. Furthermore, GLP-1 augments mitochondrial efficacy, as manifested by the ameliorated”
From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [389]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Overexpression of GLP-1 in skeletal muscle can improve endurance.”
From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [389]
The cited source says what the claim attributes to it.
In the citing paper
“Mitochondrial content and function in skeletal muscle are regulated by GLP-1.389”
From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [389]
The cited source says what the claim attributes to it.
In the citing paper
“These cellular transformations contribute significantly to enhanced endurance during exercise, thereby underscoring the critical role that GLP-1 plays in the regulation of mitochondrial function and content in skeletal muscle.389”
From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [389]
The cited source says what the claim attributes to it.
In the citing paper
“We demonstrated that GLP-1 enhances physical endurance by inducing skeletal muscle remodeling, which may be mediated by GLP-1R/AMPK signaling.389”
From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [389]
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, GLP-1 overexpression induces a myofiber-type switch towards oxidative, high-endurance muscle fibers, and also a boost of mitochondrial content and oxidative phosphorylation.”
From Adipose Tissue: A Novel Target of the Incretin Axis? A Paradigm Shift in Obesity-Linked Insulin Resistance (2024) · cites this paper as [55]
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, GLP-1 regulates skeletal muscle remodelling to enhance exercise endurance possibly via GLP-1R signalling-mediated phosphorylation of AMPK.23”
From Changes in lean body mass with glucagon‐like peptide ‐1‐based therapies and mitigation strategies (2024) · cites this paper as [23]
In the citing paper
“Additionally, other preclinical studies suggest that GLP-1 RAs may promote skeletal muscle remodeling through changes in fiber type and energy substrate utilization [12].”
From Nutrition and Physical Activity in Optimizing Weight Loss and Lean Mass Preservation in the Incretin-Based Medications Era: A Narrative Review (2025) · cites this paper as [12]
In the citing paper
“Recently, in a murine model, it has been shown that GLP-1 overexpression, in skeletal muscle, causes an increase in glycogen synthesis and induces the translocation of GLUT4 to the sarcolemma, generating augmented glucose uptake.”
From Adipose Tissue: A Novel Target of the Incretin Axis? A Paradigm Shift in Obesity-Linked Insulin Resistance (2024) · cites this paper as [55]
In the citing paper
“All things considered, these results point to the possibility that GLP-1 increases physical endurance by causing skeletal muscle remodeling [55].”
From Adipose Tissue: A Novel Target of the Incretin Axis? A Paradigm Shift in Obesity-Linked Insulin Resistance (2024) · cites this paper as [55]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Biology of Incretins: GLP-1 and GIP
Baggio, L. L., & Drucker, D. J. (2007) · Gastroenterology · doi:10.1053/j.gastro.2007.03.054 · Cited by 3,639
Fiber Types in Mammalian Skeletal Muscles
Schiaffino, S., & Reggiani, C. (2011) · Physiological Reviews · doi:10.1152/physrev.00031.2010 · Cited by 3,022
Glucagon-like peptide 1 (GLP-1)
Müller, T. D., Finan, B., Bloom, S. R., D'Alessio, D., Drucker, D. J., Flatt, P. R., Fritsche, A., Gribble, F., Grill, H. J., Habener, J. F., et al. (2019) · Molecular Metabolism · doi:10.1016/j.molmet.2019.09.010 · Cited by 1,868
Ellingsgaard, H., Hauselmann, I., Schuler, B., Habib, A. M., Baggio, L. L., Meier, D. T., Eppler, E., Bouzakri, K., Wueest, S., Muller, Y. D., et al. (2011) · Nature Medicine · doi:10.1038/nm.2513 · Cited by 922
Thorens, B. (1992) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.89.18.8641 · Cited by 906
Enteroendocrine Cells: Chemosensors in the Intestinal Epithelium
Gribble, F. M., & Reimann, F. (2016) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021115-105439 · Cited by 683
Function and mechanisms of enteroendocrine cells and gut hormones in metabolism
Gribble, F. M., & Reimann, F. (2019) · Nature Reviews Endocrinology · doi:10.1038/s41574-019-0168-8 · Cited by 670
Physiology of Proglucagon Peptides: Role of Glucagon and GLP-1 in Health and Disease
Sandoval, D. A., & D'Alessio, D. A. (2015) · Physiological Reviews · doi:10.1152/physrev.00013.2014 · Cited by 498
Richards, P., Parker, H. E., Adriaenssens, A. E., Hodgson, J. M., Cork, S. C., Trapp, S., Gribble, F. M., & Reimann, F. (2014) · Diabetes · doi:10.2337/db13-1440 · Cited by 472
Current Protocols in Microbiology
(2005) · John Wiley & Sons, Inc. eBooks · doi:10.1002/9780471729259 · Cited by 407
Cited by
Sorted by citations
Glucagon-like peptide-1 receptor: mechanisms and advances in therapy
Zheng, Z., Zong, Y., Ma, Y., Tian, Y., Pang, Y., Zhang, C., & Gao, J. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01931-z · Cited by 1,036
Changes in lean body mass with glucagon‐like peptide ‐1‐based therapies and mitigation strategies
Neeland, I. J., Linge, J., & Birkenfeld, A. L. (2024) · Diabetes, Obesity and Metabolism · doi:10.1111/dom.15728 · Cited by 391
Karakasis, P., Patoulias, D., Fragakis, N., & Mantzoros, C. S. (2025) · Metabolism · doi:10.1016/j.metabol.2024.156113 · Cited by 242
Linge, J., Birkenfeld, A. L., & Neeland, I. J. (2024) · Circulation · doi:10.1161/circulationaha.124.067676 · Cited by 180
Mechanism of action of the bile acid receptor TGR5 in obesity
Lun, W., Yan, Q., Guo, X., Zhou, M., Bai, Y., He, J., Cao, H., Che, Q., Guo, J., & Su, Z. (2023) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2023.11.011 · Cited by 122
Self-citation
Metadata
- Authors
- Wu, L., Zhou, M., Li, T., Dong, N., Yi, L., Zhang, Q., & Mi, M.
- Affiliations
- Army Medical University (CN)
- Corresponding author
- Zhang, Qianyong
- Mi, Mantian
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
- Publisher
- Elsevier BV
- Published
- 2022-09
- Volume
- 1869
- Issue
- 9
- Pages
- 119300
- ISSN
- 0167-4889 (ISSN-L)
- OpenAlex
- W4281979657
- Cited by
- 101
- References
- 39
- Citations by year
- 2026: 23 · 2025: 40 · 2024: 29 · 2023: 7 · 2022: 2
- FWCI
- 6.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 365 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81773408, AWS17J014, 81903310)
- Natural Science Foundation of Chongqing (cstc2019jcyj, 81773408, 81903310, AWS17J014, cstc2019jcyj-msxmX0201)
- Army Medical University (AWS17J014)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- glucagon-like peptide-1, exercise endurance, skeletal muscle remodeling, GLP-1 receptor, AMPK signaling, exendin-4, type I muscle fibers, mitochondrial biogenesis, glucose uptake, glycogen synthesis, metabolic syndrome
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Animals, Glucose, Mice, Inbred C57BL, Physical Conditioning, Animal, Muscle, Skeletal, Mice, Glucagon-Like Peptide 1, AMP-Activated Protein Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
