GLP-1 regulates exercise endurance and skeletal muscle remodeling via GLP-1R/AMPK pathway

Wu, Luting; Zhou, Min; Li, Tianyou; Dong, Ning; Lv, Yi; Zhang, Qianyong; Mi, Mantian

doi:10.1016/j.bbamcr.2022.119300

Cited by 30 publications

(20 citation statements)

References 39 publications

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“…It was promoted by EX4 treatment, indicating that EX4 may promote mitophagy through the activation of AMPK. A previous study showed that application of the GLP-1R agonist EX4 in skeletal muscle cells activated the AMPK pathway (Wu et al 2022 ). Another GLP-1R agonist, PF1801, inhibited muscle fiber necroptosis by activating the AMPK signaling pathway (Kamiya et al 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide-1 receptor agonist exendin 4 ameliorates diabetes-associated vascular calcification by regulating mitophagy through the AMPK signaling pathway

Chen,

Jin,

et al. 2024

Mol Med

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Background Vascular calcification (VC) is a complication in diabetes mellitus (DM) patients. Osteogenic phenotype switching of vascular smooth muscle cells (VSMCs) plays a critical role in diabetes-related VC. Mitophagy can inhibit phenotype switching in VSMCs. This study aimed to investigate the role of the glucagon-like peptide-1 receptor (GLP-1R) agonist exendin 4 (EX4) in mitophagy-induced phenotype switching. Materials and methods The status of VC in T2DM mice was monitored using Von Kossa and Alizarin Red S (ARS) staining in mouse aortic tissue. Human aortic smooth muscle cells were cultured in high glucose (HG) and β-glycerophosphate (β-GP) conditioned medium. Accumulation of LC3B and p62 was detected in the mitochondrial fraction. The effect of EX4 in vitro and in vivo was investigated by knocking down AMPKα1. Results In diabetic VC mice, EX4 decreased the percentage of von Kossa/ARS positive area. EX4 inhibited osteogenic differentiation of HG/β-GP-induced VSMCs. In HG/β-GP-induced VSMCs, the number of mitophagosomes was increased, whereas the addition of EX4 restored mitochondrial function, increased the number of mitophagosome-lysosome fusions, and reduced p62 in mitochondrial frictions. EX4 increased the phosphorylation of AMPKα (Thr172) and ULK1 (Ser555) in HG/β-GP-induced VSMCs. After knockdown of AMPKα1, ULK1 could not be activated by EX4. The accumulation of LC3B and p62 could not be reduced after AMPKα1 knockdown. Knockdown of AMPKα1 negated the therapeutic effects of EX4 on VC of diabetic mice. Conclusion EX4 could promote mitophagy by activating the AMPK signaling pathway, attenuate insufficient mitophagy, and thus inhibit the osteogenic phenotype switching of VSMCs.

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Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide-1 receptor agonist exendin 4 ameliorates diabetes-associated vascular calcification by regulating mitophagy through the AMPK signaling pathway

Chen,

Jin,

et al. 2024

Mol Med

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“…94 Insulin-like glucagon peptide 1 (GLP-1) is one of the substrates of the DPP-IV enzyme that participates in the dynamic balance of blood and promotes insulin production in the pancreas by inhibiting glucagon secretion. 95 Glucagon is a hormone secreted by the islets of the pancreas α; it is the immediate expression product of the proglucagon gene in cells. In intestinal mucosal cells, the prohormone converting enzyme cleaves proglucagon into a carboxyl-terminal peptide chain sequence, thus producing glucagon-like peptide.…”

Section: Food and Function Reviewmentioning

confidence: 99%

“…Activated GLP-1 receptor agonist (GLP-1RA) binds to GLP-1 and stimulates islet cells to secrete insulin. [92][93][94][95][96] The mechanisms of actions of CPI and its hydrolyzed peptide in lipogenesis, inflammatory response, and glucose metabolism are depicted in Fig. 3, in which, PPAR-γ and sterol regulatory element tuberculosis transcription 1 (SREBP1) jointly regulate the expression of Lp1 and other lipoproteins.…”

Section: Food and Function Reviewmentioning

confidence: 99%

A review of the functional activities of chia seed and the mechanisms of action related to molecular targets

Chen,

Wu,

Zhu

et al. 2024

Food Funct.

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“…Simultaneously, GLP-1 can improve the enhancement of insulin signalling pathway-related proteins, such as phosphorylated insulin receptor substrate 1 (IRS1) and phosphorylated AKT 61 , 169 . Furthermore, GLP-1 can promote the expression of the glycogen synthesis gene glycogen synthase 1/2 (GYS1/2) by promoting AMPK phosphorylation, and may also affect the translocation of GLUT4 to the cell membrane 170 , 171 . Furthermore, GLP-1 analogues can promote autophagy by regulating Sestrin2 (SESN2) in skeletal muscle cells, promote the expression of GLUT4 and effectively increase glucose uptake 172 ( Fig.…”

Section: Mechanism Of Action Of Tgr5 In Obesitymentioning

confidence: 99%

Mechanism of action of the bile acid receptor TGR5 in obesity

Lun,

Yan,

Guo

et al. 2024

Acta Pharmaceutica Sinica B

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GLP-1 regulates exercise endurance and skeletal muscle remodeling via GLP-1R/AMPK pathway

Cited by 30 publications

References 39 publications

Glucagon-like peptide-1 receptor agonist exendin 4 ameliorates diabetes-associated vascular calcification by regulating mitophagy through the AMPK signaling pathway

Glucagon-like peptide-1 receptor agonist exendin 4 ameliorates diabetes-associated vascular calcification by regulating mitophagy through the AMPK signaling pathway

A review of the functional activities of chia seed and the mechanisms of action related to molecular targets

Mechanism of action of the bile acid receptor TGR5 in obesity

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