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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.
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“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]
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“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]
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“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]
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“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]
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“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
“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]
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]
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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
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