Resistance training restores skeletal muscle atrophy and satellite cell content in an animal model of Alzheimer’s disease

Rahmati, Masoud; Joneydi, Mohammad Shariatzadeh; Koyanagi, Ai; Yang, Guang; Ji, Bingzhou; Lee, Seungwon; Yon, Dong Keon; Smıth, Lee; Shin, Jae Il; Li, Yusheng

doi:10.1038/s41598-023-29406-1

Cited by 18 publications

(11 citation statements)

References 30 publications

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“…According to the collaborative guidelines of the American College of Sports Medicine and the American Diabetes Association, individuals with T2DM are advised to engage in a minimum of 2–3 resistance training (RT) sessions per week, alongside AE, with moderate-to-heavy intensity [ 23 ]. RT, as a non-pharmacological intervention, has shown efficacy in improving skeletal muscle atrophy in various diseases, including diabetes, Alzheimer’s disease, and cachexia [ 24 – 26 ]. This effect can be primarily attributed to the increased activation of proteins involved in the protein synthesis pathway, particularly AKT-mTOR-p70S6K, in skeletal muscle [ 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

Exercise mitigates Dapagliflozin-induced skeletal muscle atrophy in STZ-induced diabetic rats

Yang

Wang

Zhang

et al. 2023

Diabetol Metab Syndr

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Background Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are commonly used in the management of type 2 diabetes mellitus (T2DM) and have been found to worsen the reduction of skeletal muscle mass in individuals with T2DM. This study aims to examine the potential of exercise in mitigating the skeletal muscle atrophy induced by SGLT2i treatment. Methods A rat model of T2DM (40 male Sprague-Dawley rats; T2DM induced by a combination of high-fat diet and streptozotocin) was used to examine the effects of six-week treatment with Dapagliflozin (DAPA, SGLT2i) in combination with either aerobic exercise (AE) or resistance training (RT) on skeletal muscle. T2DM-eligible rats were randomized into the T2DM control group (CON, n = 6), DAPA treatment group (DAPA, n = 6), DAPA combined with aerobic exercise intervention group (DAPA + AE, n = 6), and DAPA combined with resistance training intervention group (DAPA + RT, n = 6). To assess the morphological changes in skeletal muscle, myosin ATPase and HE staining were performed. mRNA expression levels of Atrogin-1, MuRF1, and Myostatin were determined using quantitative PCR. Furthermore, protein expression levels of AKT, p70S6K, mTOR, FoXO1/3A, NF-κB, and MuRF1 were examined through western blotting. Results Both the administration of DAPA alone and the combined exercise intervention with DAPA resulted in significant reductions in blood glucose levels and body weight in rats. However, DAPA alone administration led to a decrease in skeletal muscle mass, whereas RT significantly increased skeletal muscle mass and muscle fiber cross-sectional area. The DAPA + RT group exhibited notable increases in both total protein levels and phosphorylation levels of AKT and p70S6K in skeletal muscle. Moreover, the DAPA, DAPA + AE, and DAPA + RT groups demonstrated downregulation of protein expression (FoXO1/3A) and mRNA levels (Atrogin-1, MuRF1, and Myostatin) associated with muscle atrophy. Conclusions Our findings provide support for the notion that dapagliflozin may induce skeletal muscle atrophy through mechanisms unrelated to protein metabolism impairment in skeletal muscle, as it does not hinder protein metabolic pathways while reduces muscle atrophy-related genes. Additionally, our observations reveal that RT proves more effective than AE in enhancing skeletal muscle mass and muscle fiber cross-sectional area in rats with T2DM by stimulating protein anabolism within the skeletal muscle.

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Section: Introductionmentioning

confidence: 99%

Exercise mitigates Dapagliflozin-induced skeletal muscle atrophy in STZ-induced diabetic rats

Yang

Wang

Zhang

et al. 2023

Diabetol Metab Syndr

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“…To detect different myofibers, muscle Sects were incubated with antibodies specific to myosin heavy chain (MyHC) types I, IIa, and IIb (22280-1-AP, 55069-1-AP, and 20140-1-AP, respectively, Proteintech, Wuhan, China), unstained myofibers were judged as MyHC IIx expression. Alexa Fluor 546, CY3 and 568 secondary antibodies were used to detect MyHC types I, IIa, and IIb, respectively 52 , 53 . For each section, the average CSA of myofibers are presented as the total area of myofibers/total number of myofibers in 5 images (field of view).…”

Section: Methodsmentioning

confidence: 99%

Dietary supplementation with inulin improves burn-induced skeletal muscle atrophy by regulating gut microbiota disorders

Gao,

Zhao,

Leng

et al. 2024

Sci Rep

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Inulin, as a prebiotic, could modulate the gut microbiota. Burn injury leads to gut microbiota disorders and skeletal muscle catabolism. Therefore, whether inulin can improve burn-induced muscle atrophy by regulating microbiota disorders remains unknown. This study aimed to clarify that inulin intake alleviates gut microbiota disorders and skeletal muscle atrophy in burned rats. Rats were divided into the sham group, burn group, prebiotic inulin intervention group, and pseudo-aseptic validation group. A 30% total body surface area (TBSA) third-degree burn wound on dorsal skin was evaluated in all groups except the sham group. Animals in the intervention group received 7 g/L inulin. Animals in the validation group received antibiotic cocktail and inulin treatment. In our study inulin intervention could significantly alleviate the burn-induced skeletal muscle mass decrease and skeletal myoblast cell apoptosis. Inulin intake increased the abundances of Firmicutes and Actinobacteria but decreased the abundance of Proteobacteria. The biosynthesis of amino acids was the most meaningful metabolic pathway distinguishing the inulin intervention group from the burn group, and further mechanistic studies have shown that inulin can promote the phosphorylation of the myogenesis-related proteins PI3K, AKT and P70S6K and activate PI3K/AKT signaling for protein synthesis. In conclusion, inulin alleviated burn induced muscle atrophy through PI3K/AKT signaling and regulated gut microbiota dysbiosis.

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“…Then the membranes were incubated with goat anti-rabbit Immunoglobulin G (IgG, ab205718, 1:2500; Abcam, Cambridge, MA, USA) for 1 h. The membranes were evaluated with a Western blot (WB) kit (Sigma-Aldrich) via a Bio-Rad gel imaging system (Bio-Rad, Hercules, CA, USA). The images were analyzed with the Image J software as described by Rahmati et al 18,19 The primary antibodies included the following: anti-CTRP3 (ab36870, 1:1000; Abcam), anti-E-cadherin (ab76319, 1:1000; Abcam), anti-N-cadherin (ab76011, 1:1000; Abcam), anti-smooth muscle alpha-actin (anti-α-SMA, ab5694, 1:1000; Abcam), anti-phosphorylated (p)-p65 (3033, 1:1000; CST, Danvers, MA, USA), anti-p65 (8242, 1:1000; CST), anti-TGFβ1 (3711, 1:1000; GST), anti-p-Smad3 (9520, 1:1000; Abcam), performed by using 22G indwelling needle. After hooking up to the mouse lung function instrument, the mice were positioned on the heating plate of a closed incubator.…”

Section: Western Blot Analysismentioning

confidence: 99%

CTRP3 regulates NF-κB and TGFβ1/Smad3 pathways to alleviate airway inflammation and remodeling in asthmatic mice induced by OVA

2023

Allergol Immunopathol

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Background: Asthma is a common illness with chronic airway inflammation. C1q/tumor necrosis factor (TNF)-related protein 3 (CTRP3) plays a vital role in inflammatory response, but its effect on asthma is imprecise. Herein, we analyzed the functions of CTRP3 in asthma. Methods: The BALB/c mice were randomized into four groups: control, ovalbumin (OVA), OVA+vector, and OVA+CTRP3. The asthmatic mice model was established by OVA stimulation. Overexpression of CTRP3 was implemented by the transfection of corresponding adeno-associated virus 6 (AAV6). The contents of CTRP3, E-cadherin, N-cadherin, smooth muscle alpha-actin (α-SMA), phosphorylated (p)-p65/p65, transforming growth factor-beta 1 (TGFβ1), and p-Smad3/Smad3 were determined by Western blot analysis. The quantity of total cells, eosinophils, neutrophils, and lymphocytes in bronchoalveolar lavage fluid (BALF) was assessed by using a hemocytometer. The contents of tumor necrosis factor-α and interleukin-1β in BALF were examined by enzyme-linked immunesorbent serologic assay. The lung function indicators and airway resistance (AWR) were measured. The bronchial and alveolar structures were evaluated by hematoxylin and eosin staining and sirius red staining. Results: The CTRP3 was downregulated in mice of OVA groups; however, AAV6-CTRP3 treatment markedly upregulated the expression of CTRP3. Upregulation of CTRP3 diminished asthmatic airway inflammation by decreasing the number of inflammatory cells and the contents of proinflammatory factors. CTRP3 markedly lessened AWR and improved lung function in OVA-stimulated mice. Histological analysis found that CTRP3 alleviated OVA-induced airway remodeling in mice. Moreover, CTRP3 modulated NF-κB and TGFβ1/Smad3 pathways in OVA-stimulated mice. Conclusion: CTRP3 alleviated airway inflammation and remodeling in OVA-induced asthmatic mice via regulating NF-κB and TGFβ1/Smad3 pathways.

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Resistance training restores skeletal muscle atrophy and satellite cell content in an animal model of Alzheimer’s disease

Cited by 18 publications

References 30 publications

Exercise mitigates Dapagliflozin-induced skeletal muscle atrophy in STZ-induced diabetic rats

Exercise mitigates Dapagliflozin-induced skeletal muscle atrophy in STZ-induced diabetic rats

Dietary supplementation with inulin improves burn-induced skeletal muscle atrophy by regulating gut microbiota disorders

CTRP3 regulates NF-κB and TGFβ1/Smad3 pathways to alleviate airway inflammation and remodeling in asthmatic mice induced by OVA

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